Heightened susceptibility: A review of how pregnancy and chemical exposures influence maternal health.

Pregnancy is a unique period when biological changes can increase sensitivity to chemical exposures. Pregnant women are exposed to multiple environmental chemicals via air, food, water, and consumer products, including flame retardants, plasticizers, and pesticides. Lead exposure increases risk of pregnancy-induced hypertensive disorders, although women's health risks are poorly characterized for most chemicals. Research on prenatal exposures has focused on fetal outcomes and less on maternal outcomes. We reviewed epidemiologic literature on chemical exposures during pregnancy and three maternal outcomes: preeclampsia, gestational diabetes, and breast cancer. We found that pregnancy can heighten susceptibility to environmental chemicals and women's health risks, although variations in study design and exposure assessment limited study comparability. Future research should include pregnancy as a critical period for women's health. Incorporating biomarkers of exposure and effect, deliberate timing and method of measurement, and consistent adjustment of potential confounders would strengthen research on the exposome and women's health.

Comparing Arterial Function Parameters for the Prediction of Coronary Heart Disease Events: The Multi-Ethnic Study of Atherosclerosis (MESA).

Arterial dysfunction has been linked to decline in cardiac function and increased risk of cardiovascular disease events. We calculated the value of arterial function, measured at baseline (2000-2002), in predicting time to first coronary heart disease (CHD) event (median follow-up, 10.2 years) among participants in the Multi-Ethnic Study of Atherosclerosis (MESA). Measures included the following: C1 and C2, derived from diastolic pulse contour analysis from the radial artery blood pressure waveform obtained by tonometry (n = 6,336); carotid distensibility and Young's elastic modulus at the carotid artery, derived from carotid artery ultrasonography (n = 6,531 and 6,528); and aortic distensibility, measured using cardiac magnetic resonance imaging (n = 3,677). After adjustment, the hazard ratio for a CHD event per standard-deviation increment in arterial function was 0.97 (95% confidence interval (CI): 0.86, 1.10) for C1, 0.73 (95% CI: 0.63, 0.86) for C2, 0.98 (95% CI: 0.86, 1.11) for carotid distensibility, 0.99 (95% CI: 0.90, 1.09) for Young's modulus, and 0.90 (95% CI: 0.74, 1.10) for aortic distensibility. We examined the area under the receiver operating characteristic curve for the model with full adjustment plus the addition of each measure individually. C2 provided additional discrimination for the prediction of CHD (area under the curve = 0.736 vs. 0.743; P = 0.04). Lower C2 was associated with a higher risk of future CHD events.

Increased mortality associated with extreme-heat exposure in King County, Washington, 1980-2010.

Extreme heat has been associated with increased mortality, particularly in temperate climates. Few epidemiologic studies have considered the Pacific Northwest region in their analyses. This study quantified the historical (May to September, 1980-2010) heat-mortality relationship in the most populous Pacific Northwest County, King County, Washington. A relative risk (RR) analysis was used to explore the relationship between heat and all-cause mortality on 99th percentile heat days, while a time series analysis, using a piece-wise linear model fit, was used to estimate the effect of heat intensity on mortality, adjusted for temporal trends. For all ages, all causes, we found a 10% (1.10 (95% confidence interval (CI), 1.06, 1.14)) increase in the risk of death on a heat day versus non-heat day. When considering the intensity effect of heat on all-cause mortality, we found a 1.69% (95% CI, 0.69, 2.70) increase in the risk of death per unit of humidex above 36.0°C. Mortality stratified by cause and age produced statistically significant results using both types of analyses for: all-cause, non-traumatic, circulatory, cardiovascular, cerebrovascular, and diabetes causes of death. All-cause mortality was statistically significantly modified by the type of synoptic weather type. These results demonstrate that heat, expressed as humidex, is associated with increased mortality on heat days, and that risk increases with heat's intensity. While age was the only individual-level characteristic found to modify mortality risks, statistically significant increases in diabetes-related mortality for the 45-64 age group suggests that underlying health status may contribute to these risks.

Increased hospital admissions associated with extreme-heat exposure in King County, Washington, 1990-2010.

Increased morbidity and mortality have been associated with extreme heat events, particularly in temperate climates. Few epidemiologic studies have considered the impact of extreme heat events on hospitalization rates in the Pacific Northwest region. This study quantifies the historic (May to September 1990-2010) heat-morbidity relationship in the most populous Pacific Northwest County, King County, Washington. A relative risk (RR) analysis was used to explore the association between heat and all non-traumatic hospitalizations on 99th percentile heat days, whereas a time series analysis using a piecewise linear model approximation was used to estimate the effect of heat intensity on hospitalizations, adjusted for temporal trends and day of the week. A non-statistically significant 2% [95% CI: 1.02 (0.98, 1.05)] increase in hospitalization risk, on a heat day vs. a non-heat day, was noted for all-ages and all non-traumatic causes. When considering the effect of heat intensity on admissions, we found a statistically significant 1.59% (95% CI: 0.9%, 2.29%) increase in admissions per degree increase in humidex above 37.4°C. Admissions stratified by cause and age produced statistically significant results with both relative risk and time series analyses for nephritis and nephrotic syndromes, acute renal failure, and natural heat exposure hospitalizations. This study demonstrates that heat, expressed as humidex, is associated with increased hospital admissions. When stratified by age and cause of admission, the non-elderly age groups (<85 years) experience significant risk for nephritis and nephrotic syndromes, acute renal failure, natural heat exposure, chronic obstructive pulmonary disease, and asthma hospitalizations.

Projected health impacts of heat events in Washington State associated with climate change.

Climate change is predicted to increase the frequency and duration of extreme-heat events and associated health outcomes. This study used data from the historical heat-health outcome relationship, and a unique prediction model, to estimate mortality for 2025 and 2045. For each one degree change in humidex above threshold, we find a corresponding 1.83% increase in mortality for all ages, all non-traumatic causes of death in King County, Washington. Mortality is projected to increase significantly in 2025 and 2045 for the 85 and older age group (2.3-8.0 and 4.0-22.3 times higher than baseline, respectively).

Longitudinal effects of a decade of aging on carotid artery stiffness: the multiethnic study of atherosclerosis.

BACKGROUND AND PURPOSE: Arterial stiffening is associated with hypertension, stroke, and cognitive decline; however, the effects of aging and cardiovascular disease risk factors on carotid artery stiffening have not been assessed prospectively in a large multiethnic longitudinal study. METHODS: Distensibility coefficient and the Young's elastic modulus (YEM) of the right common carotid artery were calculated at baseline and after a mean of 9.4 (standard deviation [SD], 0.5) years in 2650 participants. Effects of age and cardiovascular disease risk factors were evaluated by multivariable mixed regression and ANCOVA models. RESULTS: At baseline, participants were 59.9 (SD, 9.4) years old (53% women; 25% black, 22% Hispanic, 14% Chinese). YEM increased from 1581 (SD, 927) to 1749 (SD, 1306) mm Hg (P<0.0001), and distensibility coefficient decreased from 3.1 (SD, 1.3) to 2.7 (SD, 1.1)×10(-3) mm Hg(-1) (P<0.001), indicating progressive arterial stiffening. YEM increased more among participants who were aged>75 years old at baseline (P<0.0001). In multivariable analyses, older age and less education independently predicted worsening YEM and distensibility coefficient. Stopping antihypertensive medication during the study period predicted more severe worsening of YEM (ß=360.2 mm Hg; P=0.008). Starting antihypertensive medication after examination 1 was predictive of improvements in distensibility coefficient (ß=1.1×10(-4) mm Hg(-1); P=0.024). CONCLUSIONS: Arterial stiffening accelerates with advanced age. Older individuals experience greater increases in YEM than do younger adults, even after considering the effects of traditional risk factors. Treating hypertension may slow the progressive decline in carotid artery distensibility observed with aging and improve cerebrovascular health.