Objective

Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States.

Methods

We linked county-specific monitoring data for particles with aerodiameter of < or = 2.5 microm (PM2.5) and < or = 10 microm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths.

Results

After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06-1.27] for a 10-mug/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category).

Conclusions

This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.

Background

Perfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals. Cross-sectional epidemiologic studies suggest PFOA is associated with liver injury biomarkers.

Objectives

We estimated associations between modeled historical PFOA exposures and liver injury biomarkers and medically validated liver disease.

Methods

Participants completed surveys during 2008-2011 reporting demographic, medical, and residential history information. Self-reported liver disease, including hepatitis, fatty liver, enlarged liver and cirrhosis, was validated with healthcare providers. Alanine aminotransferase (ALT), γ-glutamyltransferase (GGT) and direct bilirubin, markers of liver toxicity, were obtained from blood samples collected in the C8 Health Project (2005-2006). Historically modeled PFOA exposure, estimated using environmental fate and transport models and participant residential histories, was analyzed in relation to liver biomarkers (n = 30,723, including 1,892 workers) and liver disease (n = 32,254, including 3,713 workers).

Results

Modeled cumulative serum PFOA was positively associated with ALT levels (p for trend < 0.0001), indicating possible liver toxicity. An increase from the first to the fifth quintile of cumulative PFOA exposure was associated with a 6% increase in ALT levels (95% CI: 4, 8%) and a 16% increased odds of having above-normal ALT (95% CI: odds ratio: 1.02, 1.33%). There was no indication of association with either elevated direct bilirubin or GGT; however, PFOA was associated with decreased direct bilirubin. We observed no evidence of an effect of cumulative exposure (with or without a 10-year lag) on all liver disease (n = 647 cases), nor on enlarged liver, fatty liver, and cirrhosis only (n = 427 cases).

Conclusion

Results are consistent with previous cross-sectional studies showing association between PFOA and ALT, a marker of hepatocellular damage. We did not observe evidence that PFOA increases the risk of clinically diagnosed liver disease.

Citation

Darrow LA, Groth AC, Winquist A, Shin HM, Bartell SM, Steenland K. 2016. Modeled perfluorooctanoic acid (PFOA) exposure and liver function in a Mid-Ohio Valley community. Environ Health Perspect 124:1227-1233; http://dx.doi.org/10.1289/ehp.1510391.

Background

There is a growing body of epidemiologic literature reporting associations between atmospheric pollutants and reproductive outcomes, particularly birth weight and gestational duration.

Objectives

The objectives of our international workshop were to discuss the current evidence, to identify the strengths and weaknesses of published epidemiologic studies, and to suggest future directions for research.

Discussion

Participants identified promising exposure assessment tools, including exposure models with fine spatial and temporal resolution that take into account time-activity patterns. More knowledge on factors correlated with exposure to air pollution, such as other environmental pollutants with similar temporal variations, and assessment of nutritional factors possibly influencing birth outcomes would help evaluate importance of residual confounding. Participants proposed a list of points to report in future publications on this topic to facilitate research syntheses. Nested case-control studies analyzed using two-phase statistical techniques and development of cohorts with extensive information on pregnancy behaviors and biological samples are promising study designs. Issues related to the identification of critical exposure windows and potential biological mechanisms through which air pollutants may lead to intrauterine growth restriction and premature birth were reviewed.

Conclusions

To make progress, this research field needs input from toxicology, exposure assessment, and clinical research, especially to aid in the identification and exposure assessment of feto-toxic agents in ambient air, in the development of early markers of adverse reproductive outcomes, and of relevant biological pathways. In particular, additional research using animal models would help better delineate the biological mechanisms underpinning the associations reported in human studies.

Background

The findings of prior studies of air pollution effects on adverse birth outcomes are difficult to synthesize because of differences in study design.

Objectives

The International Collaboration on Air Pollution and Pregnancy Outcomes was formed to understand how differences in research methods contribute to variations in findings. We initiated a feasibility study to a) assess the ability of geographically diverse research groups to analyze their data sets using a common protocol and b) perform location-specific analyses of air pollution effects on birth weight using a standardized statistical approach.

Methods

Fourteen research groups from nine countries participated. We developed a protocol to estimate odds ratios (ORs) for the association between particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀) and low birth weight (LBW) among term births, adjusted first for socioeconomic status (SES) and second for additional location-specific variables.

Results

Among locations with data for the PM₁₀ analysis, ORs estimating the relative risk of term LBW associated with a 10-μg/m³ increase in average PM₁₀ concentration during pregnancy, adjusted for SES, ranged from 0.63 [95% confidence interval (CI), 0.30-1.35] for the Netherlands to 1.15 (95% CI, 0.61-2.18) for Vancouver, with six research groups reporting statistically significant adverse associations. We found evidence of statistically significant heterogeneity in estimated effects among locations.

Conclusions

Variability in PM₁₀-LBW relationships among study locations remained despite use of a common statistical approach. A more detailed meta-analysis and use of more complex protocols for future analysis may uncover reasons for heterogeneity across locations. However, our findings confirm the potential for a diverse group of researchers to analyze their data in a standardized way to improve understanding of air pollution effects on birth outcomes.