Time series analysis of total and direct associations between high temperatures and preterm births in Detroit, Michigan

Abstract

ObjectivesPreterm births (PTBs) represent significant health risks, and several studies have found associations between high outdoor temperatures and PTB. We estimated both the total and natural direct effects (independent of particulate matter, ozone and nitrogen dioxide air pollutants) of the prior 2-day mean apparent temperature (AT) on PTB. We evaluated effect modification by maternal age, race, education, smoking status and prenatal care.Design and settingWe obtained birth records and meteorological data for the Detroit, Michigan, USA area, for the warm months (May to September), 1991 to 2001. We used a time series Poisson regression with splines of AT, wind speed, solar radiation and citywide average precipitation to estimate total effects. To accommodate multiple mediators and exposure-mediator interactions, AT inverse odds weights, predicted by meteorological and air pollutant covariates, were added in a subsequent model to estimate direct effects.ResultsAt 24.9°C relative to 18.6°C, 10.6% (95% CI: 3.8% to 17.2%) of PTBs were attributable to the total effects of AT, and 10.4% (95% CI: 2.2% to 17.5%) to direct effects. Relative excess risks of interaction indicated that the risk of PTB with increasing temperature above 18.6°C was significantly lower among black mothers and higher among mothers less than 19, older than 30, with late or no prenatal care and who smoked.ConclusionThis additional evidence of a direct association between high temperature and PTB may motivate public health interventions to reduce extreme heat exposures among pregnant women, particularly among those who may have enhanced vulnerability.

Effect of Elevated Ambient Temperature on Maternal, Foetal, and Neonatal Outcomes: A Scoping Review

“…When environmental temperature exceeds the maternal core body temperature, it causes cutaneous vasodilation and sweat secretion, and decreases uterine and umbilical cord blood flow [10]. If heat-loss mechanisms are inadequate to dissipate heat effectively, the body becomes dehydrated [11,12]. In such conditions, the endocrine system activates and releases the antidiuretic hormone and oxytocin, further decreasing uterine blood flow to the foetus and triggering labour, often prematurely [12].…”

“…If heat-loss mechanisms are inadequate to dissipate heat effectively, the body becomes dehydrated [11,12]. In such conditions, the endocrine system activates and releases the antidiuretic hormone and oxytocin, further decreasing uterine blood flow to the foetus and triggering labour, often prematurely [12]. Heat exposure can cause acute heat stress and release heat-shock protein [13].…”

Association between maximum temperature and PM2.5 with pregnancy outcomes in Lima, Peru

“…Several studies have reported that exposure to high-temperature changes increases the risk of premature birth. 26 , 38 Heat stress could activate the fetal hypothalamic-pituitary-adrenal axis, prompting the placental release of estriol, prostaglandins which could induce labor onset. 38 …”

“… 26 , 38 Heat stress could activate the fetal hypothalamic-pituitary-adrenal axis, prompting the placental release of estriol, prostaglandins which could induce labor onset. 38 …”

Toxicant Disruption of Immune Defenses: Potential Implications for Fetal Membranes and Pregnancy

“…These include exposure to a range of toxic substances including air pollution (Liu et al, 2019), cigarette smoke (Soneji and Beltran-Sanchez, 2019), polyfluoroalkyl substances (Sagiv et al, 2018), polybrominated diphenyl ethers (PBDEs;Peltier et al, 2015), phthalate esters (Ferguson et al, 2014), lead (Taylor et al, 2015), and arsenic (Ahmad et al, 2001). Additional factors include infection with pathogenic bacteria (Bianchi-Jassir et al, 2017) and exposure to high outdoor air temperatures (Zhong et al, 2018;Gronlund et al, 2020). On a mechanistic basis, these exposures are thought to act by triggering oxidative stress and/or inflammatory pathways that are part of the normal labor process of weakening the membranes (Menon et al, 2011;Romero et al, 2014;Wallace et al, 2016;Ha et al, 2018).…”