Particulate matter exposure, dietary inflammatory index and preterm birth in Mexico city, Mexico.

BACKGROUND: Particulate matter ≤10 µm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts. OBJECTIVES: To evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks. METHODS: PM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines. RESULTS: In adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 µg/m3) during the second trimester, while negative associations were seen during the second (≥74 µg/m3) and third trimesters (55-65 µg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth. DISCUSSION: Associations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.

Air pollution and inflammation: Findings from concurrent repeated measures of systemic and reproductive tract cytokines during term pregnancy in Mexico City.

BACKGROUND: Environmental exposures are associated with a number of outcomes including adverse pregnancy outcomes. Although inflammation is hypothesized to play a role, the mechanistic pathways between environmental exposures and adverse health outcomes, including associations between exposures and longitudinal measures of systemic and reproductive tract inflammation, need elucidation. OBJECTIVES: This study was conducted to evaluate whether exposure to air pollution is associated with immunologic responses in the systemic circulation and lower reproductive tract, and to evaluate whether systemic and reproductive tract immunologic responses are similar. METHODS: We quantified repeated measures of cytokines from cervico-vaginal exudates and serum obtained concurrently among 104 women with term pregnancies and estimated PM10 and CO exposure using the monitor nearest each participant's residence. Serum and cervico-vaginal cytokines were compared using Wilcoxon signed-ranks test and Spearman rank correlations for select gestational months. We used intraclass correlation coefficients (ICCs) to quantify reproducibility of cytokine measurements, and Tobit regression to estimate associations between air pollution and cytokines. RESULTS: Median cervico-vaginal levels of IL-6, Eotaxin, IP-10, MCP-1, MIP-1α, MIP-1ß, and TNFα were higher than corresponding serum cytokines, significantly so for IL-6 and IP-10. Cervico-vaginal and serum cytokines were not correlated, but cytokines from the same fluid were correlated. ICCs for most serum cytokines were ≤0.40, while ICCs were higher in cervico-vaginal cytokines (range 0.52-0.83). IP-10 and Eotaxin had the highest ICCs for both cytokine sources. In adjusted models, PM10 was positively associated with serum cytokines IL-6, IP-10, MIP-1ß and Eotaxin but inversely associated with cervico-vaginal cytokine TNFα, IP-10, MIP-1ß, MCP-1 and Eotaxin, controlling for false discovery rate. CO was inversely associated with cervico-vaginal TNFα, IL-6, MIP-1ß, MCP-1 and Eotaxin. CONCLUSIONS: Inflammatory processes are compartment-specific. Systemic inflammatory markers may provide information on immunologic processes and response to environmental exposures, but are not proxies for lower reproductive tract inflammation.