Rt 7 – Psychiatry at QHC

Sample H&P:

HPI: 27 y/o Spanish-speaking, domiciled, married, Female with past psychiatric history of depression and anxiety and past medical history of cerebral toxoplasmosis was brought in by EMS to ED, self-activated, complaining of worsening depression, headache, and near syncopal episode earlier that day. Pt domiciled with husband in Virginia but staying with brother in Queens to pursue treatment for headaches, depression, and anxiety. Pt reports having 10/10 excruciating headaches x 4 years since diagnosis and medical treatment of cerebral toxoplasmosis 4 years ago in Virginia. Pt cannot recall the medications or name of the hospital where she received treatment. Pt reports frequent headaches, anxiety, and dizziness, and she believes she still has “cysts” in her head. Pt says she “cannot go on living like this, and I don’t care if I live or die,” but denies wanting to kill herself or having any plans to do so. Pt feels that no one believes her and her family doesn’t understand what she is going through. Pt reports compliance with Prozac 10 mg PO daily and Seroquel 100 mg PO QHS, and states she’s been taking them for “a few years.” Pt denies having seen a therapist for several months because of COVID. Pt denies taking any medication for headaches. Pt denies focal neuro Sx. Pt denies HI or hallucinations.

Writer spoke with pt’s husband Robin (571)285-8526 who confirmed history of depression and postpartum depression after their first child 7 years ago. Husband corroborates diagnosis of cerebral toxomplasmosis 4 years ago during pregnancy with their 2^nd child and reports subsequent treatment but cannot recall name of medications. Husband corroborates that pt takes her anxiety and depression meds as prescribed to the best of his knowledge.

PMHx: cerebral toxoplasmosis 4 years ago

PSHx: Denies surgical history.

PPHx: depression and anxiety x 7 years; postpartum depression x 1 year after first born son 7 years ago.

Meds: Prozac (fluoxetine) 10 mg PO daily; Seroquel (quetiapine) 100 mg PO QHS

Allergies: NKDA. Denies food or environmental allergies.

Family Hx: Noncontributory. Parents alive and well in Guatemala, no known PMHx.

Social Hx: Emigrated from Guatemala 4 years ago with husband and 2 children at the time. Now husband and 4 children live in home in Virginia, but pt staying with brother in Queens. Pt does not work. Completed some high school for education, but did not finish. No one else at home sick. No recent travel outside of country. Pt denies drinking alcohol, smoking tobacco or using tobacco products, or illicit drug use. Pt reports difficulty sleeping and diminished appetite.

ROS:

General: Fatigue

Psych: dysphoric mood, suicidal ideation.

Physical Exam:

General: Pt appears stated age. Small stature. Appropriate dress. Good hygiene.

V/S: Grossly normal.

Mental Status Exam:

General

Appearance: Pt is a short slender Guatemalan female with black hair. No visible scars or tattoos. Good hygeine. Appropriate dress. Pt appears stated age.
Behavior and Psychomotor Activity: Pt is lying in bed. Pt appears anxious and her feet and hands are fidgeting while she speaks. She maintains appropriate eye contact while talking and listening.
Attitude Towards Examiner: Pt is cooperative and she established rapport in two minutes.

Sensorium and Cognition

Alertness and Consciousness: Pt is alert and responds to verbal stimulus and when addressed.
Orientation: Pt oriented to date, place, birthday, and self.
Concentration and Attention: Pt is alert and attentive. Pt gives relevant responses to questions.
Capacity to Read and Write: Pt can read and write adequately.
Abstract Thinking: Pts ability to understand and use idioms intact. Pt able to think critically about living situation, work, family, and health.
Memory: Pt’s remote and recent memory were normal.
Fund of Information and Knowledge: Pt’s intellectual performance is marginal, but consistent with her level of education previous work experience in textiles in Guatemala.

Mood and Affect

Mood: Pt’s mood is dysphoric.
Affect: Pt’s affect sad, tearful (not sobbing), and anxious.
Appropriateness: Pt’s mood and affect are consistent with the topics discussed. She does not exhibit labile emotions, angry outbursts, or uncontrollable crying.

Motor

Speech: Pt’s speech pattern is raspy in tone and slow.
Eye Contact: Pt makes adequate eye contact.
Body Movements: Pt’s hands and feet positive for transient tremors bilaterally. Pt has no facial tics. Her body movements are decreased and slow. Pt has normal gait.

Reasoning and Control

Impulse Control: Pt’s impulse control is satisfactory. She denies suicidal or homicidal urges.
Judgment: Pt denies paranoia, delusions, auditory or visual hallucinations.
Insight: Pt has fair insight into her depression and anxiety and the need to take medications. She did not have much insight into her motivations for committing the offense.

DDx:

Bipolar disorder – Pt may be in acute depressive state of bipolar disorder.
Major Depressive Disorder – Pt exhibiting symptoms consistent with major depression
Schizoaffective disorder depressive type – While pt currently denies hallucinations, her age and preoccupation with PMHx cerebral toxoplasmosis, and social isolation may be early manifestations of schizoaffective disorder depressive type.
Latent toxoplasmosis – Pt’s PMHx of cerebral toxoplasmosis, persistent headaches, and near syncopal episode today demands that we rule out current pathologies associated with toxoplasmosis.
CVA – Pt’s reports of persistent, 10/10 excruciating headaches may be secondary to undiagnosed aneurysms or hemorrhage.

Non-contrast Head CT: Negative for significant anatomical pathology. No evidence of growths, masses, hemorrhage, or midline shift.

Assessment:

27 y/o Hispanic female with PPHx depression and anxiety and PMHx toxoplasmosis presents with acute depression and anxiety secondary to persistent 10/10 headaches.

Plan:

Admit to CPEP overnight for medication and observation. Give Tylenol 500 mg PO Q 6 hrs PRN. Increase (Prozac) fluoxetine to 20 mg PO daily for depression. Maintain Seroquel (quetiapine) at 100 mg QHS for anxiety and sleep. Consult social services for follow-up with outpatient psychiatric services (Catholic Charities) upon discharge. If symptoms persist or worsen, return to ED.

Journal Article:

Factor Structure of Cotard’s Syndrome: Systematic Review of Case Reports

Jeff Huarcaya-Victoria¹, José Bojórquez-De la Torre², Jorge De la Cruz-Oré³

Abstract

Introduction: Cotard’s syndrome is a rare psychiatric condition. As a result, current information is mainly based on reports and case series.

Objective: To analyse the psychopathological characteristics and the grouping of the symptoms of the Cotard’s syndrome cases reported in the medical literature.

Methods: A systematic review of the literature of all reported cases of Cotard’s syndrome from 2005 to January 2018 was performed in the MEDLINE/PubMed database. Demographic variables and clinical characteristics of each case were collected. An exploratory factor analysis of the symptoms was performed.

Results: The search identified 86 articles, of which 69 were potentially relevant. After reviewing the full texts, 55 articles were selected for the systematic review, in which we found 69 cases. We found that the diagnosis of major depression (P<0.001) and organic mental disorder (P=0.004) were more frequent in the older group with Cotard’s syndrome. An exploratory factor analysis extracted 3 factors: psychotic depression, in which it includes patients with delusions of guilt (0.721), suicidal ideas (0.685), delusions of damnation (0.662), nihilistic delusions of the body (0.642), depression (0.522), and hypochondriacal delusions (0.535); delusive-hallucinatory, with patients who presented delusions of immortality (0.566), visual hallucinations (0.545) and nihilistic delusions of existence (0.451), and mixed, with patients who presented nihilistic delusions of concepts (0.702), anxiety (0.573), and auditory hallucinations (0.560).

Conclusions: The psychopathology of Cotard’s syndrome is more complex than the simple association with the delusion of being dead, since it encompasses a factorial structure organized into 3 factors.

Site Eval Presentation Summary:

Our site evaluations were online via Zoom with Dr. Emanuel Saint Martin. As there were only two of us students for this rotation period, we were able to have a more in-depth discussion about our cases, pharmacology, and our articles. I felt that my written H&P’s were up to the standards of the CPEP EMR’s at QHC, and Dr. Saint Martin said that he could tell both myself and my classmate are nearing the end of our clinical year based on the depth and quality of our H&P’s. I think that my verbal presentation of my cases wen’t smoothly. Dr. Saint Martin left encouraging feedback that prompted me to look up more information about my differential diagnoses, especially as they related to specific types of delusional disorders and organic causes of delirium.

Typhon Totals:

Typhon Totals Psych

Self-Reflection:

Psychiatry is an interesting corner of medicine. This rotation felt like stepping into another world of patient interviewing and pharmacology. I feel that this rotation challenged many of my stereotypes about mental health, particularly substance abuse, that I wasn’t even fully aware of before Day 1. The CPEP is a unique environment as well. It can be full of shouting and activity, even more so than a busy medical ER. It’s an intimidating environment at first. It was difficult to engage with patients who were not my own because many times they would keep you detained with questions that I couldn’t know the answer to, usually about discharge or when their provider would be available to speak to them.

One seemingly obvious observation about these patients is that none of them were born as they are. This is something that is easy to understand intellectually, but it’s another to experience this through direct observation and engaging with these patients for prolonged periods of time. They didn’t suddenly appear on this planet floridly schizophrenic or addicted to alcohol or methamphetamine. Moreover, each of these patients is someone’s child, sibling, spouse, or parent. Collateral information plays a very important role in history-taking in the CPEP and is a constant reminder that each patient is someone’s family. I would spend anywhere from 5 to 15 minutes at a time talking to each patients’ emergency contacts to get more context about their psych and medical history and the events that led them to the CPEP. It was not uncommon for family members to express confusion, fear, sadness, or even guilt over the phone, especially if this was a new patient without a previously diagnosis. Family members of our more established patients, the “frequent fliers”, sounded tired or frustrated over the phone. Obtaining collateral information was a uniquely sensitive and important aspect of CPEP.

As the weeks went by, I became much more comfortable with both the patients as well as the pharmacology, which is mostly unique to psychiatric patient populations. I still feel as though I have a lot to learn, especially about different personality disorders, but I sense that will come with more time and experience. I do feel much better equipped to recognize and empathize with psychiatric patients now, whether I continue to work in psych or as I come across these patients in other specialties.

CAT Final:

A 26 y/o F G2P1001 presents for her first prenatal wellness exam at 4 wks EGA. She’s worried about “city” air quality having negative effects on her child’s development. On further questioning, she relates that her family has recently moved to the NY metropolitan area for work, and they’re not accustomed to increased emissions and particulate matter in the air. While there is no established family history of asthma, CHD, or adverse outcomes at birth, she is still concerned about potential risks associated with airborne pollutants.

Search Question: Is there an established correlation between airborne pollutants associated with increased emissions and adverse neonatal health outcomes?

Question Type:

☒Prevalence ☐Screening ☐Diagnosis

☒Prognosis ☐Treatment ☒Harms

PICO search terms:

P	I	C	O
Newborns	Maternal exposure		Fetal Development
Infants	Prenatal exposure		Birth Weight
Neonatal	Air Quality Index (AQI)		Birth Height
	Air pollution		Adverse perinatal outcomes
	PM_2.5		IUGR
	PM₁₀		Congenital heart disease
	Emissions		Asthma

Search tools and strategy used:

PubMed

Maternal exposure pollutants fetal development  3608
- Filters: 5 years, meta-analysis, systematic review, RCT  28
  - 1 year  5
- Air quality fetal development  758
  - Filters: 10 years, meta-analysis, systematic review  19
    - 1 year  2
  - 5 fetal development  59
    - Filter: 1 year  7
  - Particulate matter fetal development  640
    - Filter: systematic review, meta-analysis, RCT, 5 years  14

Cochrane

Air quality fetal development  7081
- Child Health  Neonatal Care  Other Neonatal  40
Maternal exposure pollutants fetal development  3146
- Child Health  Neonatal Care  Other Neonatal  26

Trip

Maternal exposure pollutants  508
- Since 2016  242
  - 7 Systematic Reviews, 4 control trials
- Air Quality fetal development  652
  - Since 2016  180
    - 13 Systematic reviews

As this is a potentially very broad topic, I’ve decided to revisit this discussion with a few specific neonatal outcomes in mind: anthropometrics, neonatal respiratory status, cardiovascular and respiratory development, and perinatal adverse events. There are numerous systematic reviews and meta-analyses that investigate prenatal exposure to poor air quality/pollution/emissions/particulate matter, but do not evaluate for the types of outcomes that my CAT is specifically asking.

There is also the related, but not entirely appropriate, topic of maternal health and peripartum outcomes. While I consider those equally important, I am opting to exclude those studies if they do not serve to answer my original question about fetal health outcomes.

As before, I will also be excluding those studies which focus on long-term behavioral and psychosocial outcomes as those cannot be assessed for at birth and involve more qualitative than quantitative criteria.

I’ve included sources from my previous PICO, but I’ve also expanded my search criteria to include sources that will further elucidate the relationship between specific types of pollutants (PM_2.5, PM₁₀, CO, O₃, NO₂, and SO₂) and their implications in intrauterine growth restriction (IUGR), respiratory devo, cardiovascular devo, and perinatal health outcomes.

Articles Chosen

Article 1:

Citation:

Katie C Hall¹², Jennifer C Robinson¹². Association between maternal exposure to pollutant particulate matter 2.5 and congenital heart defects: a systematic review. JBI Database System Rev Implement Rep. 2019 Aug;17(8):1695-1716.

PMID: 31021973

PMCID: PMC6707530

DOI: 10.11124/JBISRIR-2017-003881

Type of Article:

Systematic Review

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707530/pdf/nihms-1046581.pdf

Abstract:

Objective: The objective of this review was to determine if there was an association between maternal exposure to pollutant particulate matter 2.5 during the first trimester of pregnancy and congenital heart defects within the first year of life.

Introduction: The environment is recognized as an important determinant of health for both the individual and population. Air pollution specifically is a major environmental risk factor impacting health with links to asthma, heart disease, obesity, and fetal developmental complications. Of the commonly monitored air pollutants, particulate matter 2.5 has associations with health, especially among vulnerable populations such as children and pregnant women. A congenital heart defect is a fetal complication that impacts 34.3 million infants globally, with more than 80% of the diagnoses having an unknown etiology. Although environmental risk factors such as air pollution are thought to be a risk factor in the diagnosis of a congenital heart defect, epidemiologic research evidence is limited.

Inclusion criteria: This review considered studies that evaluated maternal exposure to the air pollutant particulate matter 2.5 during the first trimester (weeks 1-12) of fetal development. The primary outcome was a diagnosis of a congenital heart defect in an infant within the first year of life.

Methods: A three-step search strategy was utilized in this review and included 11 databases and two websites. Studies published from January 2002 to September 2018 were eligible for inclusion. Only papers published in English were included. Eligible studies underwent critical appraisal by two independent reviewers using standardized critical appraisal instruments from JBI. Quantitative data were extracted from the included studies independently by two reviewers. Odds ratios (ORs) and 95% confidence intervals (CIs) were extracted for the individual outcome measures, specifically atrial septal defect, ventricular septal defect, and tetralogy of fallot, respectively. The defects were identified and pooled, where possible, in statistical meta-analysis. Where statistical pooling was not possible, findings were reported narratively.

Results: Five studies were identified that met the inclusion criteria, including three cohort and two case-control designs. Each individual study identified at least one statistically significant increase or inverse association between particulate matter 2.5 and a congenital heart defect. An increased risk was identified with more than seven isolated and two groupings of congenital heart defects. An inverse risk was identified with two isolated and one grouping of congenital heart defects. Meta-analysis results were: atrial septal defect, OR = 0.65 (95% CI, 0.37 to 1.15); ventricular septal defect, OR = 1.02 (95% CI, 075 to 1.37); and tetralogy of fallot, OR = 1.16 (95% CI, 0.78 to 1.73), indicating no statistically significant findings.

Conclusion: There was no significant evidence to support an association between air pollutant particulate matter 2.5 and a congenital heart defect in the first year of life. However, few studies met the rigorous inclusion criteria, and the studies that did had high heterogeneity, making it difficult to complete a meta-analysis with such a limited number of articles. Further research is needed to standardize the outcomes and pollutant monitoring methods, and provide comparable analysis results so that future synthesis of the literature can be conducted.

Article 2:

Citation:

Zhijuan Cao¹, Lulu Meng¹, Yan Zhao¹, Chao Liu², Yingying Yang¹, Xiujuan Su¹, Qingyan Fu³, Dongfang Wang³, Jing Hua⁴. Maternal exposure to ambient fine particulate matter and fetal growth in Shanghai, China. Environ Health. 2019 May 16;18(1):49. PMID: 31096994. PMCID: PMC6524254. DOI: 10.1186/s12940-019-0485-3

Type of Article:

Prospective Cohort

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524254/pdf/12940_2019_Article_485.pdf

Abstract:

Background: Fetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM_2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.

Methods: A total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM_2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM_2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO₂, NO₂, PM₁₀ and O₃) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).

Results: The full model showed that with each 10 μg/m³ increase in PM_2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, – 1.91), 5.57 (- 6.66, – 4.47), and 5.47 (- 6.39, – 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, – 13.49) grams by Hadlock’s third formula and 13.56 (- 14.71, – 12.50) grams by Shepard’s formula with each 10 μg/m³ increase in PM_2.5 exposure.

Conclusions: A negative correlation existed between maternal PM_2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Article 3:

Citation:

Indulaxmi Seeni¹, Sandie Ha², Carrie Nobles¹, Danping Liu³, Seth Sherman⁴, Pauline Mendola⁵. Air pollution exposure during pregnancy: maternal asthma and neonatal respiratory outcomes. Ann Epidemiol. 2018 Sep;28(9):612-618.e4. Epub 2018 Jun 13.

PMID: 30153910 PMCID: PMC6232679 DOI: 10.1016/j.annepidem.2018.06.003

Type of Article:

Retrospective cohort

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6232679/pdf/nihms-995400.pdf

Abstract:

Purpose: Maternal asthma increases adverse neonatal respiratory outcomes, and pollution may further increase risk. Air quality in relation to neonatal respiratory health has not been studied.

Methods: Transient tachypnea of the newborn (TTN), asphyxia, and respiratory distress syndrome (RDS) were identified using medical records among 223,375 singletons from the Consortium on Safe Labor (2002-2008). Community Multiscale Air Quality models estimated pollutant exposures. Multipollutant Poisson regression models calculated adjusted relative risks of outcomes for interquartile range increases in average exposure. Maternal asthma and preterm delivery were evaluated as effect modifiers.

Results: TTN risk increased after particulate matter (PM) less than or equal to 10-micron exposure during preconception and trimester one (9-10%), and whole-pregnancy exposure to PM less than or equal to 2.5 microns (PM_2.5; 17%) and carbon monoxide (CO; 10%). Asphyxia risk increased after exposure to PM_2.5 in trimester one (48%) and whole pregnancy (84%), CO in trimester two and whole pregnancy (28-32%), and consistently for ozone (34%-73%). RDS risk was associated with increased concentrations of nitrogen oxides (33%-42%) and ozone (9%-21%) during all pregnancy windows. Inverse associations were observed with several pollutants, particularly sulfur dioxide. No interaction with maternal asthma was observed. Restriction to term births yielded similar results.

Conclusions: Several pollutants appear to increase neonatal respiratory outcome risks.

Article 4:

Citation:

Milena Jacobs¹, Guicheng Zhang², Shu Chen², Ben Mullins², Michelle Bell³, Lan Jin³, Yuming Guo⁴, Rachel Huxley², Gavin Pereira². The association between ambient air pollution and selected adverse pregnancy outcomes in China: A systematic review. Sci Total Environ. 2017 Feb 1;579:1179-1192. Epub 2016 Nov 29. PMID: 27913015 PMCID: PMC5252829 DOI: 10.1016/j.scitotenv.2016.11.100

Type of Article:

Systematic Review

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5252829/pdf/nihms833175.pdf

Abstract:

The association between exposure to ambient air pollution and respiratory or cardiovascular endpoints is well-established. An increasing number of studies have shown that this exposure is also associated with adverse pregnancy outcomes. However, the majority of research has been undertaken in high-income western countries, with relatively lower levels of exposure. There is now a sufficient number of studies to warrant an assessment of effects in China, a relatively higher exposure setting. We conducted a systematic review of 25 studies examining the association between ambient air pollution exposure and adverse pregnancy outcomes (lower birth weight, preterm birth, mortality, and congenital anomaly) in China, published between 1980 and 2015. The results indicated that sulphur dioxide (SO₂) was more consistently associated with lower birth weight and preterm birth, and that coarse particulate matter (PM₁₀) was associated with congenital anomaly, notably cardiovascular defects.

Article 5:

Citation:

Dries S Martens¹, Bianca Cox¹, Bram G Janssen¹, Diana B P Clemente¹²³, Antonio Gasparrini⁴⁵, Charlotte Vanpoucke⁶, Wouter Lefebvre⁷, Harry A Roels¹⁸, Michelle Plusquin¹, Tim S Nawrot¹⁹. Prenatal Air Pollution and Newborns’ Predisposition to Accelerated Biological Aging. JAMA Pediatrics. 2017 Dec 1;171(12):1160-1167. doi: 10.1001/jamapediatrics.2017.3024. PMID: 29049509. PMCID: PMC6233867.

Type of Article:

Prospective Cohort

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233867/pdf/emss-80385.pdf

Abstract:

Importance: Telomere length is a marker of biological aging that may provide a cellular memory of exposures to oxidative stress and inflammation. Telomere length at birth has been related to life expectancy. An association between prenatal air pollution exposure and telomere length at birth could provide new insights in the environmental influence on molecular longevity.

Objective: To assess the association of prenatal exposure to particulate matter (PM) with newborn telomere length as reflected by cord blood and placental telomere length.

Design, setting, and participants: In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 2014, all with a singleton full-term birth (≥37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere lengths were included, resulting in a final study sample size of 641.

Exposures: Maternal residential PM2.5 (particles with an aerodynamic diameter ≤2.5 μm) exposure during pregnancy.

Main outcomes and measures: In the newborns, cord blood and placental tissue relative telomere length were measured. Maternal residential PM2.5 exposure during pregnancy was estimated using a high-resolution spatial-temporal interpolation method. In distributed lag models, both cord blood and placental telomere length were associated with average weekly exposures to PM2.5 during pregnancy, allowing the identification of critical sensitive exposure windows.

Results: In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, -14.1% to -3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, -19.3% to -6.7%) shorter placental telomere length. These associations were controlled for date of delivery, gestational age, maternal body mass index, maternal age, paternal age, newborn sex, newborn ethnicity, season of delivery, parity, maternal smoking status, maternal educational level, pregnancy complications, and ambient temperature.

Conclusions and relevance: Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere length. The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length during life. Therefore, improvements in air quality may promote molecular longevity from birth onward.

Article 6:

Citation:

Qiong Wang¹²³, Bing Li⁴, Tarik Benmarhnia⁵⁶, Shakoor Hajat⁷⁸, Meng Ren¹, Tao Liu⁹, Luke D Knibbs¹⁰, Huanhuan Zhang¹¹¹, Junzhe Bao¹, Yawei Zhang¹², Qingguo Zhao¹³, Cunrui Huang¹²³¹¹. Independent and Combined Effects of Heatwaves and PM_2.5 on Preterm Birth in Guangzhou, China: A Survival Analysis. Environ Health Perspectives. 2020 Jan;128(1):17006. doi: 10.1289/EHP5117. Epub 2020 Jan 7. PMID: 31909654. PMCID: PMC7015562.

Type of Article:

Retrospective Cohort

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015562/pdf/ehp-128-017006.pdf

Abstract:

Background: Both extreme heat and air pollution exposure during pregnancy have been associated with preterm birth; however, their combined effects are unclear.

Objectives: Our goal was to estimate the independent and joint effects of heatwaves and fine particulate matter [PM <2.5μm<2.5μm in aerodynamic diameter (PM2.5PM2.5)], exposure during the final gestational week on preterm birth.

Methods: Using birth registry data from Guangzhou, China, we included 215,059 singleton live births in the warm season (1 May-31 October) between January 2015 and July 2017. Daily meteorological variables from 5 monitoring stations and PM2.5 concentrations from 11 sites were used to estimate district-specific exposures. A series of cut off temperature thresholds and durations (2, 3, and 4 consecutive d) were used to define 15 different heatwaves. Cox proportional hazard models were used to estimate the effects of heatwaves and PM2.5PM2.5 exposures during the final week on preterm birth, and departures from additive joint effects were assessed using the relative excess risk due to interaction (RERI).

Results: Numbers of preterm births increased in association with heatwave exposures during the final gestational week. Depending on the heatwave definition used, hazard ratios (HRs) ranged from 1.10 (95% CI: 1.01, 1.20) to 1.92 (1.39, 2.64). Associations were stronger for more intense heatwaves. Combined effects of PM2.5PM2.5 exposures and heatwaves appeared to be synergistic (RERIs>0RERIs>0) for less extreme heatwaves (i.e., shorter or with relatively low temperature thresholds) but were less than additive (RERIs<0RERIs<0) for more intense heatwaves.

Conclusions: Our research strengthens the evidence that exposure to heatwaves during the final gestational week can independently trigger preterm birth. Moderate heatwaves may also act synergistically with PM2.5PM2.5 exposure to increase risk of preterm birth, which adds new evidence to the current understanding of combined effects of air pollution and meteorological variables on adverse birth outcomes. https://doi.org/10.1289/EHP5117.

Article 7:

Citation:

Yuan-Yuan Wang¹², Qin Li¹³, Yuming Guo⁴⁵, Hong Zhou¹³, Xiaobin Wang⁶⁷, Qiaomei Wang⁸, Haiping Shen⁸, Yiping Zhang⁸, Donghai Yan⁸, Ya Zhang², Hongguang Zhang², Shanshan Li⁵, Gongbo Chen⁵, Jun Zhao², Yuan He², Ying Yang², Jihong Xu², Yan Wang², Zuoqi Peng², Hai-Jun Wang¹³, Xu Ma¹². Association of Long-term Exposure to Airborne Particulate Matter of 1 μm or Less With Preterm Birth in China. JAMA Pediatrics. 2018 Mar 5;172(3):e174872. doi: 10.1001/jamapediatrics.2017.4872. Epub 2018 Mar 5. PMID: 29297052. PMCID: PMC5885853.

Type of Article:

National Cohort Study

Article PDF:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5885853/

Abstract:

Importance: Airborne particulate matter pollution has been associated with preterm birth (PTB) in some studies. However, most of these studies assessed only populations living near monitoring stations, and the association of airborne particulate matter having a median diameter of 1 μm or less (PM₁) with PTB has not been studied.

Objective: To evaluate whether PM₁ concentrations are associated with the risk of PTB.

Design, setting, and participants: This national cohort study used National Free Preconception Health Examination Project data collected in 324 of 344 prefecture-level cities from 30 provinces of mainland China. In total, 1,300,342 healthy singleton pregnancies were included from women who were in labor from December 1, 2013, through November 30, 2014. Data analysis was conducted between December 1, 2016, and April 1, 2017.

Exposures: Predicted weekly PM₁ concentration data collected using satellite remote sensing, meteorologic, and land use information matched with the home addresses of pregnant women.

Main outcomes and measures: Preterm birth (<37 gestational weeks). Gestational age was assessed using the time since the first day of the last menstrual period. Cox proportional hazards regression analysis was used to examine the associations between trimester-specific PM₁ concentrations and PTB after controlling for temperature, seasonality, spatial variation, and individual covariates.

Results: Of the 1,300,342 singleton live births at the gestational age of 20 to 45 weeks included in this study, 104,585 (8.0%) were preterm. In fully adjusted models, a PM₁ concentration increase of 10 μg/m3 over the entire pregnancy was significantly associated with increased risk of PTB (hazard ratio [HR], 1.09; 95% CI, 1.09-1.10), very PTB as defined as gestational age from 28 through 31 weeks (HR, 1.20; 95% CI, 1.18-1.23), and extremely PTB as defined as 20 through 27 weeks’ gestation (HR, 1.29; 95% CI, 1.25-1.34). Pregnant women who were older (30-50 years) at conception (HR, 1.13; 95% CI, 1.11-1.14), were overweight before pregnancy (HR, 1.13; 95% CI, 1.11-1.15), had a rural household registration (HR, 1.09; 95% CI, 1.09-1.10), worked as farmers (HR, 1.10; 95% CI, 1.09-1.11), and conceived in autumn (HR, 1.48; 95% CI, 1.46-1.50) appeared to be more sensitive to PM₁ exposure than their counterparts.

Conclusions and relevance: Results from this national cohort study examining more than 1.3 million births indicated that exposure to PM₁ air pollution was associated with an increased risk of PTB in China. These findings will provide evidence to inform future research studies, public health interventions, and environmental policies.

Summary of the Evidence:

Author (Date)	Level of Evidence	Sample/Setting (# of subjects/ studies, cohort definition etc. )	Outcome(s) studied	Key Findings	Limitations and Biases
Hall, KC & Robinson, JC (2019)	Systematic Review	Prenatal exposure to PM_2.5 5 studies met inclusion criteria (3 cohorts, 2 case controls)	Presence of congenital heart defects within first year of life (specifically atrial septal defect, ventricular septal defect, and tetralogy of fallot)	There was no significant evidence to support an association between air pollutant particulate matter 2.5 and a congenital heart defect in the first year of life.	Few studies met the rigorous inclusion criteria, and the studies that did had high heterogeneity, making it difficult to complete a meta-analysis with such a limited number of articles. Further research is needed to standardize the outcomes and pollutant monitoring methods, and provide comparable analysis results so that future synthesis of the literature can be conducted. The authors do not specify any biases or conflicts of interest.
Cao, et al (2019)	Prospective Cohort	7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015.	Weekly average PM_2.5 values from 53 monitors Repeated fetal ultrasound measurements during gestational weeks 14-40 were selected. Estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas.	With each 10 μg/m³ increase in PM_2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, – 1.91), 5.57 (- 6.66, – 4.47), and 5.47 (- 6.39, – 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, – 13.49) grams by Hadlock’s third formula and 13.56 (- 14.71, – 12.50) grams by Shepard’s formula with each 10 μg/m³ increase in PM_2.5 exposure. A negative correlation existed between maternal PM_2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.	There were some limitations to this study. First, the maternal active and passive smoking status were not investigated. However, according to a previous study, the proportion of pregnant women who actively smoke is very low (nearly 2%) [31], and the passive rate during pregnancy was 7.8% [32] in Shanghai, China. Second, we were unable to determine more detailed maternal activity patterns beyond simple residential location, and thus, exposure estimates will suffer some misclassification. However, much of the mismeasurement is likely to be random in terms of pollution exposure. Third, socioeconomic status (SES) was not collected. Individuals with a deferent SES background may take different protection behaviors for air pollution (i.e., wearing masks and using air purifiers). In this study, registered residence and staff medical insurance were used to reflect the SES level indirectly. Authors deny any biases or conflict of interest.
Seeni, et al. (2018)	Retrospective cohort	223,385 singleton births greater than or equal to 23 weeks of gestation in the Consortium on Safe Labor (2002–2008), a retrospective cohort study using electronic medical records (EMRs) conducted across 12 U.S. clinical sites, which included 15 hospital referral regions with 19 hospitals	Transient Tachypnea in Newborns (TTN), Respiratory Distress Syndrome (RDS), and Asphyxia	Several pollutants appear to increase neonatal respiratory outcome risks. TTN risk increased after particulate matter (PM) less than or equal to 10-micron exposure during preconception and trimester one (9–10%), and whole-pregnancy exposure to PM less than or equal to 2.5 microns (PM2.5; 17%) and carbon monoxide (CO; 10%). Asphyxia risk increased after exposure to PM2.5 in trimester one (48%) and whole pregnancy (84%), CO in trimester two and whole pregnancy (28–32%), and consistently for ozone (34%–73%). RDS risk was associated with increased concentrations of nitrogen oxides (33%–42%) and ozone (9%–21%) during all pregnancy windows. Inverse associations were observed with several pollutants, particularly sulfur dioxide. No interaction with maternal asthma was observed. Restriction to term births yielded similar results.	This is the first study to investigate the relations between air pollution, maternal asthma, and neonatal respiratory outcomes. This study has several limitations. First, air pollution exposure for each mother was estimated based on the hospital referral region, which varied in size. Although this method may introduce some nondifferential exposure misclassification, it also assesses a broader geographic area that helped account for residential mobility and daily activity patterns that were not available in our data. However, the model did adjust for region, which reduces variability and potentially bias our results toward the null. Although a strength of our study was our ability to evaluate different windows of exposure, the window-specific findings may be somewhat influenced by the correlation of exposure across time windows. Whole pregnancy averages avoid this concern when evaluating chronic exposure risks. There were also few cases of asphyxia distributed across study sites, which limited certain analyses, such as the truncated whole-pregnancy exposure analysis for term neonates. Finally, we observed intermittent inverse associations, such as those between PM10 and asphyxia, which remain unexplained. The authors do not specify any biases or conflicts of interest.
Jacobs, et al. (2016)	Systematic Review	25 studies examining the association between ambient air pollution exposure and adverse pregnancy outcomes (lower birth weight, preterm birth, mortality, and congenital anomaly) in China, published between 1980 and 2015. Of the 25 reviewed studies, the majority were conducted in large urban areas. Seven studies were based in the Guangdong province (including Guangzhou) and five were in Beijing. The most common study design was case-control (nine studies), followed by cross-sectional (eight studies). There were only two prospective cohort studies and both were conducted in Beijing.	Association between ambient air pollutant exposure (NO₂, SO₂, CO, PM₁₀, PM_2.5 and ozone (O₃)) and the following adverse pregnancy outcomes in China: decrease in birth weight, low birth weight, preterm birth, mortality and congenital anomaly.	Sulphur dioxide (SO₂) was more consistently associated with lower birth weight and preterm birth. Coarse particulate matter (PM₁₀) was associated with congenital anomaly, notably cardiovascular defects.	This is the first systematic review of the association between ambient air pollution and adverse pregnancy outcomes in China. Only a few studies adjusted for smoking as a risk factor, but smoking rates among women living in Chinese cities are generally very low. None of the reviewed studies undertook personal monitoring or satellite remote sensing. Measurement error may differ by study due to differences in the monitoring network or spatial heterogeneity of pollutant by study area. We attempted to mitigate publication bias by including articles written in Chinese. The study population in China differs in some aspects from the study populations in western countries. Notably, the rate of preterm birth differs for Chinese-born women living China versus those living in different countries, which may be due to factors such as smoking and sexual practices. The authors do not specify any biases or conflicts of interest.
Martens, et al. (2017)	Prospective Cohort	In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 2014, all with a singleton full-term birth (≥37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere lengths were included, resulting in a final study sample size of 641.	In the newborns, cord blood and placental tissue relative telomere length (TL) were measured.	In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM_2.5 exposure during mid-gestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-μg/m3 increment in PM_2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, −14.1% to −3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, −19.3% to −6.7%) shorter placental telomere length.	To our knowledge, this study is the first to report an association between prenatal exposure to PM_2.5 air pollution and TL at birth, both in cord blood and placental tissue. Our results are based on exposure at the maternal residence, and potential misclassification may be present because we could not account for other exposure sources that contribute to personal exposure, such as exposure during a commute, at work, and elsewhere. The assessment of TL at birth represents a specific snapshot in the gestational period. We were not able to evaluate telomere dynamics throughout the entire pregnancy period, and, in view of our results, the role of telomerase needs further evaluation. Parental TL may be a determinant of the initial telomere length setting of the next generation. Because parents exposed to PM_2.5 may have shorter telomeres, the association between PM_2.5 exposure and newborn TL may be mediated by parental TLs. This study was funded in part by the Flemish Science Fund and the Medical Science Fund UK. The authors do not specify any biases or conflicts of interest.
Wang, et al. (2020)	Retrospective Cohort	Using birth registry data from Guangzhou, China, we included 215,059 singleton live births in the warm season (1 May-31 October) between January 2015 and July 2017.	Birth Preterm Outcomes (PTB), defined as delivery prior to 37 completed weeks of gestation, classified into moderate-to-late PTB (32 to 37 weeks), very PTB (28 to 32 weeks), and extremely PTB (less than 28 weeks). Meteorological variables, including daily mean and maximum temperature [in degrees Celsius (°C)] as well as relative humidity (%) from five meteorological stations, were collected from Guangdong Meteorological Service Center Daily ambient air pollutant concentrations (in micrograms per cubic meter) for the entire study period, including PM₁₀, PM_2.5, NO₂, SO₂, and O₃.	Numbers of preterm births increased in association with heatwave exposures during the final gestational week. Associations were stronger for more intense heatwaves. Combined effects of PM_2.5 exposures and heatwaves appeared to be synergistic (RERIs>0RERIs>0) for less extreme heatwaves (i.e., shorter or with relatively low temperature thresholds) but were less than additive (RERIs<0RERIs<0) for more intense heatwaves.	To the best of our knowledge, this study is the first to evaluate both independent effects of heatwave exposure during the last gestational week on PTB and its potential interactive effects with PM_2.5 exposure. This study has several potential limitations. Exposure misclassification could be present due to the lack of information on the exact residential address, maternal activity patterns, and residential mobility during pregnancy. Moreover, we were unable to estimate the effects of heatwaves or air pollution on spontaneous and medically indicated PTB subtypes due to the lack of this information in our data. We also did not use multipollutant models because of the moderate-to-high correlation between air pollutants in this study. Therefore, the potential confounding by other pollutants could not be assessed. Further, we were unable to consider several potentially important modifying factors, including the presence of cervicovaginal or intrauterine infections, specific prenatal complications (preeclampsia, eclampsia, gestational diabetes mellitus), socioeconomic status, maternal exercise, smoking, and nutritional status because these variables were not available in the birth registry system This study was supported by grants from National Key R&D Program of China (2018YFA0606200), National Natural Science Foundation of China (81602819), Fundamental Research Funds for the Central Universities (19ykpy88), and Guangdong Provincial Natural Science Foundation Team Project (2018B030312005). This study was also supported by Overlook International Foundation.
Wang, et al. (2018)	National Cohort Study	National Free Preconception Health Examination Project data collected in 324 of 344 prefecture-level cities from 30 provinces of mainland China. In total, 1,300,342 healthy singleton pregnancies were included from women who were in labor from December 1, 2013, through November 30, 2014.	Preterm birth (<37 gestational weeks). Gestational age was assessed using the time since the first day of the last menstrual period. Cox proportional hazards regression analysis was used to examine the associations between trimester-specific PM₁ concentrations and PTB after controlling for temperature, seasonality, spatial variation, and individual covariates.	PM₁concentration increase of 10 μg/m³ over the entire pregnancy was significantly associated with increased risk of PTB, very PTB (28 to 31 wks), and extremely PTB (20 to 27 wks). Pregnant women who were older (30-50 years) at conception, overweight before pregnancy, had a rural household registration, worked as farmers, and conceived in autumn appeared to be more sensitive to PM₁ exposure than their counterparts.	To our knowledge, no study has reported associations between PM₁ and PTB, very PTB, or extremely PTB. There could have been misclassification of the exposure. The pollutant levels at microenvironmental levels (eg, indoor, outdoor, or associated with commuting) or maternal activity patterns may contribute to misclassification. Specific components and their proportions could not be considered separately but rather were grouped as PM₁. The specific components might have had different chemical structures and might be associated with different health concerns. Future studies are needed to investigate PM components and their sources. No conflicts of interest disclosed.

Article Conclusions:

Hall & Robinson (2019): This systematic review directly addresses the relationship between air quality and neonatal outcomes, specifically prenatal exposure to fine particulate matter (PM_2.5) and congenital heart defects (CHD). The authors of this systematic review and meta-analysis found that there was conflicting and highly heterogenous evidence that might indicate a relationship between PM_2.5 and CHD. At this time the evidence is not sufficient to support that claim, and further studies of more rigorous standards are needed to elucidate such a relationship.

Cao, et al (2019): This cohort study has a large sample size (n=7965) and specifically addresses the relationship between air quality (PM_2.5) and objective anthropometric outcomes at birth (fetal weight, abdominal circumference, and femur length). One potential drawback is that this study was conducted in Shanghai, so there may be numerous environmental, genetic, or socioeconomic confounders that limit the applicability of these findings to US populations. The authors concluded that a negative correlation exists between maternal PM_2.5 exposure and fetal growth indicators. In other words, the evidence suggests that increased levels of PM_2.5 exposure may correlate directly with increased fetal growth restriction.

Seeni, et al (2018): This retrospective cohort study was recently conducted in the US and has a very large sample size (n = 223,375) derived from EMR’s of numerous clinical sites across the country. This study aimed to establish a relationship between prenatal air pollution exposure (PM₁₀, PM_2.5, CO, NO₂, SO₂, and O₃) and maternal and fetal respiratory outcomes. The primary focus regarding neonatal outcomes were the incidence of transient tachypnea in newborns (TTN), asphyxia, and respiratory distress syndrome (RDS). This study not only distinguishes between the different types of airborne pollutants being studied, but also adjusts for timing and duration of exposure during pregnancy (based on trimesters). PM_2.5 was found to directly correlate with TTN and asphyxia; CO directly correlates with TTN, asphyxia, and RDS; and ozone (O₃) directly correlates with asphyxia and RDS. NO₂ also directly correlated with RDS.

Jacobs, et al (2016): This recent systematic review focuses on the relationship between prenatal exposure to various air pollutants and adverse outcomes in pregnancy. However, this study was conducted in China, and it may have limited applicability to US populations. This study concludes that there is a consistent association between sulphur dioxide (SO₂) and preterm birth as well as low birth weight. The study also notes an association between course particulate matter (PM₁₀) and cardiovascular defects.

Martens, et al (2017): This prospective cohort is recent and it does answer my question, but in a way that I did not anticipate going into this topic. This study found that increased exposure to PM_2.5 correlated with a statistically significant decrease in telomere length of leukocytes in cord blood and placenta at birth. A few drawbacks to this study is that there is potentially significant implications for development later in life, but these findings do not currently correlate with immediately measurable neonatal outcomes which is the focus of this CAT. It is a very interesting subject personally, and it will be exciting to see what the significance of these findings are with cohesive long-term follow-up.

Wang, et al (2020): This cohort had a very large sample size (n = 215,059 ) but it only indirectly answers my question, as the focus of this study was on the relationship between heatwaves near time of delivery and preterm births. It also surveyed PM2.5 exposure during the same time period in order to evaluate for preterm outcomes during heatwaves both with and without the added effects of PM_2.5 exposure. This study found that heatwaves had a significant effect on preterm births during the week leading up to labor, and PM_2.5 played a more significant role in preterm labor during less severe heatwaves. There did not appear to be any additive effect by PM2.5 exposure during significant heatwaves. This study was also conducted in China and may have limited applicability to US populations.

Wang, et al (2018): This cohort had the largest sample size of any of my other sources included in this CAT (n = 1,300,342). This study sourced data from 324 prefecture cities around China. It posits a very significant correlation between PM₁ exposure throughout pregnancy and increased risk of preterm labor. While the findings in Chinese populations may have limited applicability to US populations, the authors posit that their access to studies published in Chinese was useful in mitigating publication bias that US or Western studies may come upon.

Overall Conclusion:

Among the most studied forms of airborne pollutants that I came across, PM_2.5 seems to have the most statistically significant correlation with decreased birth weight, transient tachypnea in newborns (TTN), and preterm labor. It relationship with RDS and CHD is not well established. Yet to be determined is the clinical significance of the apparent decrease in telomere length that is associated with PM_2.5 exposure in neonatal leukocytes found in cord blood and placenta.

More so than PM_2.5, there may be an even stronger association between preterm delivery and PM₁, but more studies are needed to establish that relationship.

Increased exposure to CO, NO₂, and O₃ are also associated with poor neonatal respiratory status.

One study found that there is a strong association between SO₂ and preterm birth. Incidentally, another study focused on neonatal respiratory outcomes found SO₂ to have an inverse relationship with poor neonatal respiratory status, and the authors of that study speculate that this may be due SO₂’s effect on a cellular respiratory pathway that may inhibit the formation of reactive oxygen species. This is not well understood though.

Many of these articles claim that they are the first of their kind to be elucidating these specific relationships between specific airborne pollutant associated with urban emission and neonatal birth weight, respiratory status, and preterm delivery.

Weight of Evidence:

1) Hall & Robinson (2019): I would give this article the most weight as it is very recent and is a systematic review. It offers a focused study on the relationship between PM2.5 and CHD, but states that there is not a clear relationship between the two at this time.

2) Jacobs, et al (2016): I would weigh this article as second most significant as it is also a systematic review and relatively recent. This article posits a strong correlation between SO₂ exposure and preterm birth as well as low birth weight. It also states that there may be a correlation between PM₁₀ and CHD, but it is not well established at this time.

3) Seeni, et al (2018): I would weigh this article as the most significant of the cohorts that I’ve included. It has a very large sample size and does a thorough job of explaining the observed relationships between various fetal respiratory outcomes at delivery (TTN, RDS, and asphyxia) and exposure to PM₁₀, PM_2.5, CO, NO₂, SO₂, and O₃.

4) Wang, et al (2018): I would weigh this article as the most significant of the cohort studies. It has by far the largest sample size and it directly deals with prenatal exposure to PM₁ and preterm birth outcomes.

5) Wang, et al (2020): I would weigh this as the second most important cohort because it is the most recent and also has a very large sample size. This study focused on the relationship between prenatal exposure to PM_2.5 and preterm birth outcomes.

6) Cao, et al (2019): I would not give this cohort as much weight as the others given its small sample size. This article does clearly establish a correlation between PM_2.5 exposure throughout pregnancy and fetal growth restriction assessed via ultrasound at weekly intervals from 14 to 40 wks gestation.

7) Martens, et al (2017): I’d give this cohort the least weight for the CAT. It has a relatively small sample size and it does not necessarily translate to clinically significant outcomes at this time. It does establish a new and interesting correlation between increased PM2.5 exposure and decreased telomere length which may have implications for future health outcomes in neonates.

Magnitude of any effects: While there is increasing statistically significant evidence that prenatal exposure to airborne pollutants, particularly PM_2.5, are associated with fetal growth restriction, increased incidence of adverse respiratory outcomes, and increased rate of preterm delivery, it does not necessarily change my clinical decision-making or guidance for expectant mothers in the NY metropolitan area. Further studies are needed to establish the impact of these airborne pollutants at levels that correlate with those of New York and other large cities in the US because at this time most of the primary information available comes from studies being conducted in large cities across China whose air quality indices (AQI’s) differ greatly from those of NY. This currently limits the applicability of these studies to US populations.

Clinical bottom line:

At this time, it would be prudent to advise expectant mothers to continue regular prenatal care appointments as directed by their OB/Gyn and to not pursue any drastic life changes (such as moving) that might impact their regular prenatal care.

There are numerous studies of varying quality that corroborate the claim that prenatal exposure to airborne pollutants, especially PM_2.5, have a direct association with lower birth weight, IUGR, and preterm delivery. There is strong evidence to suggest a direct relationship between air quality and adverse neonatal respiratory events. There is conflicting evidence of congenital heart disease associated with air quality.s

While many of the studies conducted in China posit a direct relationship between poor air quality and low birth weight and respiratory illness, it is important to keep in mind that the air quality index (AQI) of some of the cities that these studies are conducted in (eg Beijing and Shanghai) have average PM_2.5 levels that are greater than 4x that of the New York metropolitan area.

There are publicly available online resources for monitoring air quality such as airnow.gov or aqicn.org, but I would not advise parents to worry about monitoring the AQI with any regularity.

Links to Full Sources:

1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707530/pdf/nihms-1046581.pdf

2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524254/pdf/12940_2019_Article_485.pdf

3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6232679/pdf/nihms-995400.pdf

4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5252829/pdf/nihms833175.pdf

5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233867/pdf/emss-80385.pdf

6) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015562/pdf/ehp-128-017006.pdf

7) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5885853/

PANCE Prep Plan:

If the remainder of our clinical rotations continue as planned, then I would give myself roughly 4 weeks after rotations to fully focus on studying. This would put my PANCE date around early-mid March.

After reviewing the 2019 PANCE Blueprint, here’s the breakdown by body system:

Cardiovascular 13%

Pulmonary 10%

GI 9%

Musculoskeletal 8%

Endocrine, EENT, Neuro, Reproductive 7% (each)

ID, Psych 6% (each)

Derm, GU, Renal, Heme 5% (each)

Towards the end of Clinical Rotations:

My last 2 rotations are surgery and LTC. During surgery, I will most likely be fully occupied with the scheduling demands of the rotation itself and trying to prepare specifically for the EORE. However, I plan on using my time in LTC to go back through Pance Prep Pearls to study not only for the EORE, but lay the groundwork for my PANCE study plan after rotations. I will go straight through PPP over those 5 weeks.

Week 1 (after last EORE):

The day after my last EORE for LTC, I will make my own 200-question exams on both Rosh Review and Kaplan. I will use the results of those practice test to inform my first week of studying. I will spend the next 5 days (roughly 8 hrs/day) outlining the topics that I performed weakest on, and review those topics specifically in PPP and Osmosis.

At the end of the week I will make focused 50-question exams on those specific topics in both Kaplan and Rosh Review. I will review those results and highlight that material moving forward through PPP for extra review as needed.

Week 2:

This will be the week for reviewing Cardiovascular, Pulmonary, GI, Musculoskeletal, Endocrine, and EENT systems in PPP.

I will make 2 more 100-question exams on both Rosh and Kaplan with these body systems, review results and highlight material in Pance Prep Pearls. Through the rest of the week, I will spend roughly 2 days on Cardio, 1 day on Pulm, 1 day on GI, 1 day on Musculoskeletal, and 1 day on both Endo and ENT.

Near the end of the week, I will go back through the material that I underperformed on my practice exams for each of these body systems.

Week 3:

This will be my week to review Neuro, Repro, ID, Psych, Derm, GU, Renal and Heme systems in PPP.

Like before, I will make 2 exams, 100-question each, on Kaplan and Rosh Review selecting for those body systems. I will note my weakest areas and make the appropriate highlights to PPP.

Going through PPP, I will spend 1 day Neuro and Repro, 1 day on ID and Psych, 1 day on Derm and GU, and 1 day on Renal and Heme.

I will go back to Kaplan and Rosh, review the questions I got wrong again, and retake those exams.

Week 4:

I will use this week to go back through my weakest areas from each test, pharmacology, and a quick review of the 3 “high yield systems” (CV, Pulm, GI).

I will give myself 3 days to review all of our Pharmacology PowerPoints, 2 days to review Cardio/Pulm/GI, and 1 day for a final practice exams, 100 questions each, on Kaplan and Rosh Review.

Last day before PANCE:

Get up early, have a big breakfast, go for a hike, have a big dinner, and go to bed early!

CV and Sample Cover Letter:

Erik Oatman PA-S Cover Letter

Erik Oatman PA-S CV 2020

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Rt 7 – Psychiatry at QHC

Sample H&P:

Journal Article:

Factor Structure of Cotard’s Syndrome: Systematic Review of Case Reports

Abstract

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Self-Reflection:

CAT Final:

PANCE Prep Plan:

CV and Sample Cover Letter:

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