Air Pollution and Mortality in the Medicare Population

Air Pollution Still Kills

By Rebecca E. Berger, M.D., Ramya Ramaswami, M.B., B.S., M.P.H., Caren G. Solomon, M.D., M.P.H., and Jeffrey M. Drazen, M.D. Article, Metrics11 References, 10 Citing Articles

In late October 1948, a dense smog descended over the town of Donora, Pennsylvania. The town was home to a zinc plant and a steel mill, both run by the United States Steel Corporation. Susan Gnora, a 62-year-old resident of Donora, started to gasp and cough as the smog descended.1 She died the next day. Dr. William Rongaus, a physician and a member of the board of health, went door to door, treating patients for their respiratory symptoms and encouraging them to leave town if they could. Many thousands were ill, and at least 20 people died in one of the worst air-pollution disasters in U.S. history. The Donora tragedy transformed our perception of smog from a nuisance to a potential killer.

We started to improve air quality with the Clean Air Act of 1963. In 1970, Richard Nixon established the Environmental Protection Agency (EPA) by executive order, and the Clean Air Act was amended to institute National Ambient Air Quality Standards (NAAQS), which set exposure limits for six major air pollutants.2 Among the pollutants regulated by the EPA is fine particulate matter — inhalable particles with an aerodynamic diameter of less than 2.5 μm (PM2.5). Major contributors to PM2.5 in the United States include various types of transportation and the coal-fired generation of electricity.3,4 Since the 1970s, hundreds of articles have been written establishing an association between PM2.5 and poor health outcomes, including asthma, ischemic heart disease, and all-cause mortality in urban populations.5,6 In response to these findings, regulators have lowered NAAQS for the allowable amount of PM2.5 in the air.7 Current NAAQS, last updated in 2012, set an annual mean PM2.5 level of 12 μg per cubic meter. This standard, which is to be reviewed every 5 years, aims to protect the population, especially those who are particularly sensitive to the adverse effects of air pollution, including children, elderly persons, and persons with cardiopulmonary disease.2 As communities meet these stricter standards, fewer people will become sick and die as a result of air pollution. A 2011 report from the EPA projected that by 2020, amendments to the Clean Air Act would prevent more than 230,000 premature deaths, largely as a result of reductions in PM2.5 levels.8 But are current standards sufficient to protect public health?

Di et al. now report in the Journal the results of a large study, including more than 60 million Medicare beneficiaries from the years 2000 through 2012, that addresses the association between annual average levels of PM2.5 and ozone,9 as measured at the ZIP Code level, and mortality. For every increase of 10 μg per cubic meter in PM2.5, there was an associated 7.3% increase in all-cause mortality (95% confidence interval [CI], 7.1 to 7.5), after adjustment for demographic characteristics, Medicaid eligibility, and area-level covariates. Below the current NAAQS for PM2.5 of 12 μg per cubic meter, the data showed that each increase in PM2.5 of 10 μg per cubic meter was associated with an even greater increase (13.6%) in mortality (95% CI, 13.1 to 14.1). There was no appreciable level below which the risk of death tapered off — and thus no “safe” level of PM2.5. Owing to the large size of the cohort, Di et al. were able to perform robust subgroup analyses and identified greater risks of death associated with air pollutants among blacks and Medicaid-eligible populations; moreover, these groups were more likely to be exposed to higher pollutant levels.

The findings of Di et al. stress the need for tighter regulation of air-pollutant levels, including the imposition of stricter limits on levels of PM2.5. Despite compelling data, the Trump administration is moving headlong in the opposite direction. In March, Trump signed an executive order that lifted a moratorium on new leases for coal mined on public and tribal lands and began a process to dismantle guidelines intended to reduce emissions from coal-fired electricity plants.10 Earlier this month, he announced his intention to withdraw the United States from the Paris climate agreement. Although these actions were primarily intended to undo efforts made by the Obama administration to address climate change, the potentially dire consequences also include increasing people’s exposure to particulate matter. In addition, EPA Administrator Scott Pruitt has not ruled out the possibility of revoking a waiver included in the 1970 Clean Air Act that allows California to set limits on automotive tailpipe emissions that are more stringent than national standards11; 15 states have adopted California’s standards. Revoking this waiver could have the effect of exposing more than 100 million Americans to higher levels of automobile emissions. Trump’s proposed budget includes crippling cuts to the EPA, including cuts in funding for both federal and state enforcement of regulations. The increased air pollution that would result from loosening current restrictions would have devastating effects on public health.

In explaining his withdrawal from the Paris climate agreement, Trump stated, “I was elected to represent the citizens of Pittsburgh, not Paris.” Ironically, Pittsburgh is less than 30 miles from the Donora Smog Museum, where a sign reads, “Clean Air Started Here.” With the report by Di et al. adding to the large body of evidence indicating the risks of air pollution, even at current standards, we must redouble our commitment to clean air. If such protections lapse, Americans will suffer and we are doomed to repeat history. Do we really want to breathe air that kills us?

June 29, 2017 N Engl J Med 2017; 376:2591-2592 DOI: 10.1056/NEJMe1706865

  • Qian Di, M.S., 
  • Yan Wang, M.S., 
  • Antonella Zanobetti, Ph.D., 
  • Yun Wang, Ph.D., 
  • Petros Koutrakis, Ph.D., 
  • Christine Choirat, Ph.D., 
  • Francesca Dominici, Ph.D., 
  • and Joel D. Schwartz, Ph.D.

Studies have shown that long-term exposure to air pollution increases mortality. However, evidence is limited for air-pollution levels below the most recent National Ambient Air Quality Standards. Previous studies involved predominantly urban populations and did not have the statistical power to estimate the health effects in underrepresented groups.

We constructed an open cohort of all Medicare beneficiaries (60,925,443 persons) in the continental United States from the years 2000 through 2012, with 460,310,521 person-years of follow-up. Annual averages of fine particulate matter (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM2.5]) and ozone were estimated according to the ZIP Code of residence for each enrollee with the use of previously validated prediction models. We estimated the risk of death associated with exposure to increases of 10 μg per cubic meter for PM2.5 and 10 parts per billion (ppb) for ozone using a two-pollutant Cox proportional-hazards model that controlled for demographic characteristics, Medicaid eligibility, and area-level covariates.

RESULTS

Increases of 10 μg per cubic meter in PM2.5 and of 10 ppb in ozone were associated with increases in all-cause mortality of 7.3% (95% confidence interval [CI], 7.1 to 7.5) and 1.1% (95% CI, 1.0 to 1.2), respectively. When the analysis was restricted to person-years with exposure to PM2.5 of less than 12 μg per cubic meter and ozone of less than 50 ppb, the same increases in PM2.5 and ozone were associated with increases in the risk of death of 13.6% (95% CI, 13.1 to 14.1) and 1.0% (95% CI, 0.9 to 1.1), respectively. For PM2.5, the risk of death among men, blacks, and people with Medicaid eligibility was higher than that in the rest of the population.

CONCLUSIONS

In the entire Medicare population, there was significant evidence of adverse effects related to exposure to PM2.5 and ozone at concentrations below current national standards. This effect was most pronounced among self-identified racial minorities and people with low income. (Supported by the Health Effects Institute and others.)

QUICK TAKEAir Pollution and Mortality 02:03

The adverse health effects associated with long-term exposure to air pollution are well documented.1,2 Studies suggest that fine particles (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM2.5]) are a public health concern,3 with exposure linked to decreased life expectancy.4-6 Long-term exposure to ozone has also been associated with reduced survival in several recent studies, although evidence is sparse.4,7-9

Studies with large cohorts have investigated the relationship between long-term exposures to PM2.5 and ozone and mortality4,9-13; others have estimated the health effects of fine particles at low concentrations (e.g., below 12 μg per cubic meter for PM2.5).14-18 However, most of these studies have included populations whose socioeconomic status is higher than the national average and who reside in well-monitored urban areas. Consequently, these studies provide limited information on the health effects of long-term exposure to low levels of air pollution in smaller cities and rural areas or among minorities or persons with low socioeconomic status.

To address these gaps in knowledge, we conducted a nationwide cohort study involving all Medicare beneficiaries from 2000 through 2012, a population of 61 million, with 460 million person-years of follow-up. We used a survival analysis to estimate the risk of death from any cause associated with long-term exposure (yearly average) to PM2.5 concentrations lower than the current annual National Ambient Air Quality Standard (NAAQS) of 12 μg per cubic meter and to ozone concentrations below 50 parts per billion (ppb). Subgroup analyses were conducted to identify populations with a higher or lower level of pollution-associated risk of death from any cause.

Methods

MORTALITY DATA

We obtained the Medicare beneficiary denominator file from the Centers for Medicare and Medicaid Services, which contains information on all persons in the United States covered by Medicare and more than 96% of the population 65 years of age or older. We constructed an open cohort consisting of all beneficiaries in this age group in the continental United States from 2000 through 2012, with all-cause mortality as the outcome. For each beneficiary, we extracted the date of death (up to December 31, 2012), age at year of Medicare entry, year of entry, sex, race, ZIP Code of residence, and Medicaid eligibility (a proxy for low socioeconomic status). Persons who were alive on January 1 of the year following their enrollment in Medicare were entered into the open cohort for the survival analysis. Follow-up periods were defined according to calendar years.

ASSESSMENT OF EXPOSURE TO AIR POLLUTION

Ambient levels of ozone and PM2.5 were estimated and validated on the basis of previously published prediction models.19,20 Briefly, we used an artificial neural network that incorporated satellite-based measurements, simulation outputs from a chemical transport model, land-use terms, meteorologic data, and other data to predict daily concentrations of PM2.5 and ozone at unmonitored locations. We fit the neural network with monitoring data from the Environmental Protection Agency (EPA) Air Quality System (AQS) (in which there are 1928 monitoring stations for PM2.5 and 1877 monitoring stations for ozone). We then predicted daily PM2.5 and ozone concentrations for nationwide grids that were 1 km by 1 km. Cross-validation indicated that predictions were good across the entire study area. The coefficients of determination (R2) for PM2.5 and ozone were 0.83 and 0.80, respectively; the mean square errors between the target and forecasting values for PM2.5 and ozone were 1.29 μg per cubic meter and 2.91 ppb, respectively. Data on daily air temperature and relative humidity were retrieved from North American Regional Reanalysis with grids that were approximately 32 km by 32 km; data were averaged annually.21

For each calendar year during which a person was at risk of death, we assigned to that person a value for the annual average PM2.5 concentration, a value for average ozone level during the warm season (April 1 through September 30), and values for annual average temperature and humidity according to the ZIP Code of the person’s residence. The warm-season ozone concentration was used to compare our results with those of previous studies.10 In this study, “ozone concentration” refers to the average concentration during the warm season, unless specified otherwise.

As part of a sensitivity analysis, we also obtained data on PM2.5 and ozone concentrations from the EPA AQS and matched that data with each person in our study on the basis of the nearest monitoring site within a distance of 50 km. (Details are provided in Section 1 in the Supplementary Appendix, available with the full text of this article at NEJM.org.)

STATISTICAL ANALYSIS

Table 1.Cohort Characteristics and Ecologic and Meteorologic Variables.

We fit a two-pollutant Cox proportional-hazards model with a generalized estimating equation to account for the correlation between ZIP Codes.22 In this way, the risk of death from any cause associated with long-term exposure to PM2.5 was always adjusted for long-term exposure to ozone, and the risk of death from any cause associated with long-term exposure to ozone was always adjusted for long-term exposure to PM2.5, unless noted otherwise. We also conducted single-pollutant analyses for comparability. We allowed baseline mortality rates to differ according to sex, race, Medicaid eligibility, and 5-year categories of age at study entry. To adjust for potential confounding, we also obtained 15 ZIP-Code or county-level variables from various sources and a regional dummy variable to account for compositional differences in PM2.5 across the United States (Table 1, and Section 1 in the Supplementary Appendix). We conducted this same statistical analysis but restricted it to person-years with PM2.5 exposures lower than 12 μg per cubic meter and ozone exposures lower than 50 ppb (low-exposure analysis) (Table 1, and Section 1 in the Supplementary Appendix).

To identify populations at a higher or lower pollution-associated risk of death from any cause, we refit the same two-pollutant Cox model for some subgroups (e.g., male vs. female, white vs. black, and Medicaid eligible vs. Medicaid ineligible). To estimate the concentration-response function of air pollution and mortality, we fit a log-linear model with a thin-plate spline of both PM2.5 and ozone and controlled for all the individual and ecologic variables used in our main analysis model (Section 7 in the Supplementary Appendix). To examine the robustness of our results, we conducted sensitivity analyses and compared the extent to which estimates of risk changed with respect to differences in confounding adjustment and estimation approaches (Sections S2 through S4 in the Supplementary Appendix).

Data on some important individual-level covariates were not available for the Medicare cohort, including data on smoking status, body-mass index (BMI), and income. We obtained data from the Medicare Current Beneficiary Survey (MCBS), a representative subsample of Medicare enrollees (133,964 records and 57,154 enrollees for the period 2000 through 2012), with individual-level data on smoking, BMI, income, and many other variables collected by means of telephone survey. Using MCBS data, we investigated how the lack of adjustment for these risk factors could have affected our calculated risk estimates in the Medicare cohort (Section 5 in the Supplementary Appendix). The computations in this article were run on the Odyssey cluster, which is supported by the FAS Division of Science, Research Computing Group, and on the Research Computing Environment, which is supported by the Institute for Quantitative Social Science in the Faculty of Arts and Sciences, both at Harvard University. We used R software, version 3.3.2 (R Project for Statistical Computing), and SAS software, version 9.4 (SAS Institute).

Results

COHORT ANALYSES

The full cohort included 60,925,443 persons living in 39,716 different ZIP Codes with 460,310,521 person-years of follow-up. The median follow-up was 7 years. The total number of deaths was 22,567,924. There were 11,908,888 deaths and 247,682,367 person-years of follow-up when the PM2.5 concentration was below 12 μg per cubic meter and 17,470,128 deaths and 353,831,836 person-years of follow-up when the ozone concentration was below 50 ppb. These data provided excellent power to estimate the risk of death at air-pollution levels below the current annual NAAQS for PM2.5 and at low concentrations for ozone (Table 1).Figure 1.Average PM2.5 and Ozone Concentrations in the Continental United States, 2000 through 2012.

Annual average PM2.5 concentrations across the continental United States during the study period ranged from 6.21 to 15.64 μg per cubic meter (5th and 95th percentiles, respectively), and the warm-season average ozone concentrations ranged from 36.27 to 55.86 ppb (5th and 95th percentiles, respectively). The highest PM2.5 concentrations were in California and the eastern and southeastern United States. The Mountain region and California had the highest ozone concentrations; the eastern states had lower ozone concentrations (Figure 1).Table 2.Risk of Death Associated with an Increase of 10 μg per Cubic Meter in PM2.5 or an Increase of 10 ppb in Ozone Concentration.

In a two-pollutant analysis, each increase of 10 μg per cubic meter in annual exposure to PM2.5 (estimated independently of ozone) and each increase of 10 ppb in warm-season exposure to ozone (estimated independently of PM2.5) was associated with an increase in all-cause mortality of 7.3% (95% confidence interval [CI], 7.1 to 7.5) and 1.1% (95% CI, 1.0 to 1.2), respectively. Estimates of risk based on predictive, ZIP-Code–specific assessments of exposure were slightly higher than those provided by the nearest data-monitoring site (Table 2). When we restricted the PM2.5 and ozone analyses to location-years with low concentrations, we continued to see significant associations between exposure and mortality (Table 2). Analysis of the MCBS subsample provided strong evidence that smoking and income are not likely to be confounders because they do not have a significant association with PM2.5 or ozone (Section 5 in the Supplementary Appendix).

SUBGROUP ANALYSES

Figure 2.Risk of Death Associated with an Increase of 10 μg per Cubic Meter in PM2.5 Concentrations and an Increase of 10 ppb in Ozone Exposure, According to Study Subgroups.Figure 3.Concentration–Response Function of the Joint Effects of Exposure to PM2.5 and Ozone on All-Cause Mortality.

Subgroup analyses revealed that men; black, Asian, and Hispanic persons; and persons who were eligible for Medicaid (i.e., those who had low socioeconomic status) had a higher estimated risk of death from any cause in association with PM2.5 exposure than the general population. The risk of death associated with ozone exposure was higher among white, Medicaid-eligible persons and was significantly below 1 in some racial subgroups (Figure 2). Among black persons, the effect estimate for PM2.5 was three times as high as that for the overall population (Table S3 in the Supplementary Appendix). Overall, the risk of death associated with ozone exposure was smaller and somewhat less robust than that associated with PM2.5 exposure. We also detected a small but significant interaction between ozone exposure and PM2.5 exposure (Table S8 in the Supplementary Appendix). Our thin-plate–spline fit indicated a relationship between PM2.5, ozone, and all-cause mortality that was almost linear, with no signal of threshold down to 5 μg per cubic meter and 30 ppb, respectively (Figure 3, and Fig. S8 in the Supplementary Appendix).

Discussion

This study involving an open cohort of all persons receiving Medicare, including those from small cities and rural areas, showed that long-term exposures to PM2.5 and ozone were associated with an increased risk of death, even at levels below the current annual NAAQS for PM2.5. Furthermore, the study showed that black men and persons eligible to receive Medicaid had a much higher risk of death associated with exposure to air pollution than other subgroups. These findings suggest that lowering the annual NAAQS may produce important public health benefits overall, especially among self-identified racial minorities and people with low income.

The strengths of this study include the assessment of exposure with high spatial and temporal resolution, the use of a cohort of almost 61 million Medicare beneficiaries across the entire continental United States followed for up to 13 consecutive years, and the ability to perform subgroup analyses of the health effects of air pollution on groups of disadvantaged persons. However, Medicare claims do not include extensive individual-level data on behavioral risk factors, such as smoking and income, which could be important confounders. Still, our analysis of the MCBS subsample (Table S6 in the Supplementary Appendix) increased our level of confidence that the inability to adjust for these individual-level risk factors in the Medicare cohort did not lead to biased results (Section 5 in the Supplementary Appendix). In another study, we analyzed a similar Medicare subsample with detailed individual-level data on smoking, BMI, and many other potential confounders linked to Medicare claims.23 In that analysis, we found that for mortality and hospitalization, the risks of exposure to PM2.5 were not sensitive to the additional control of individual-level variables that were not available in the whole Medicare population.

We also found that our results were robust when we excluded individual and ecologic covariates from the main analysis (Fig. S2 and Table S2 in the Supplementary Appendix), when we stratified age at entry into 3-year and 4-year categories rather than the 5 years used in the main analysis (Fig. S3 in the Supplementary Appendix), when we varied the estimation procedure (by means of a generalized estimating equation as opposed to mixed effects) (Tables S3 and S4 in the Supplementary Appendix), and when we used different types of statistical software (R, version 3.3.2, vs. SAS, version 9.4). Finally, we found that our results were consistent with others published in the literature (Section 6 in the Supplementary Appendix).5,17,24-28

There was a significant association between PM2.5 exposure and mortality when the analysis was restricted to concentrations below 12 μg per cubic meter, with a steeper slope below that level. This association indicated that the health-benefit-per-unit decrease in the concentration of PM2.5 is larger for PM2.5 concentrations that are below the current annual NAAQS than the health benefit of decreases in PM2.5 concentrations that are above that level. Similar, steeper concentration-response curves at low concentrations have been observed in previous studies.29 Moreover, we found no evidence of a threshold value — the concentration at which PM2.5 exposure does not affect mortality — at concentrations as low as approximately 5 μg per cubic meter (Figure 3); this finding is similar to those of other studies.18,30

The current ozone standard for daily exposure is 70 ppb; there is no annual or seasonal standard. Our results strengthen the argument for establishing seasonal or annual standards. Moreover, whereas time-series studies have shown the short-term effects of ozone exposure, our results indicate that there are larger effect sizes for longer-term ozone exposure, including in locations where ozone concentrations never exceed 70 ppb. Unlike the American Cancer Society Cancer Prevention Study II,9,10 our study reported a linear connection between ozone concentration and mortality. This finding is probably the result of the interaction between PM2.5 and ozone (Section 7 in the Supplementary Appendix). The significant, linear relationship between seasonal ozone levels and all-cause mortality indicates that current risk assessments,31-33 which incorporate only the acute effects of ozone exposure on deaths each day from respiratory mortality, may be substantially underestimating the contribution of ozone exposure to the total burden of disease.

The enormous sample size in this study, which includes the entire Medicare cohort, allowed for unprecedented accuracy in the estimation of risks among racial minorities and disadvantaged subgroups. The estimate of effect size for PM2.5 exposure was greatest among male, black, and Medicaid-eligible persons. We also estimated risks in subgroups of persons who were eligible for Medicaid and in whites and blacks alone to ascertain whether the effect modifications according to race and Medicaid status were independent. We found that black persons who were not eligible for Medicaid (e.g., because of higher income) continued to have an increased risk of death from exposure to PM2.5 (Fig. S4 in the Supplementary Appendix). In addition, we found that there was a difference in the health effects of PM2.5 exposure between urban and rural populations, a finding that may be due to compositional differences in the particulates (Table S3 Supplementary Appendix).

Although the Medicare cohort includes only the population of persons 65 years of age or older, two thirds of all deaths in the United States occur in people in that age group. Although our exposure models had excellent out-of-sample predictive power on held-out monitors, they do have limitations. Error in exposure assessment remains an issue in this type of analysis and could attenuate effect estimates for air pollution.34

The overall association between air pollution and human health has been well documented since the publication of the landmark Harvard Six Cities Study in 1993.25 With air pollution declining, it is critical to estimate the health effects of low levels of air pollution — below the current NAAQS — to determine whether these levels are adequate to minimize the risk of death. Since the Clean Air Act requires the EPA to set air-quality standards that protect sensitive populations, it is also important to focus more effort on estimating effect sizes in potentially sensitive populations in order to inform regulatory policy going forward.

Supported by grants from the Health Effects Institute (4953-RFA14-3/16-4), the National Institutes of Health (R01 ES024332-01A1, ES-000002, ES024012, R01ES026217), the National Cancer Institute (R35CA197449), and the Environmental Protection Agency (83587201-0 and RD-83479801).

**

August 2020

Study Links Gas Flares to Preterm Births, With Hispanic Women at High Risk

Expectant mothers who lived near flaring sites had higher odds of giving birth prematurely than those who did not, researchers found. The adverse outcomes fell entirely on Hispanic women.

A flare in Loving County, Texas. Energy companies flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable.
A flare in Loving County, Texas. Energy companies flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable.Credit…Angus Mordant/Reuters

By Julia Rosen

  • Published July 22, 2020Updated July 23, 2020

Across the United States, gas flares light the night skies over oil and gas fields — visible symbols of the country’s energy boom. They also emit greenhouse gases, making them symbols of climate change that many environmental groups would like to see snuffed out.

Now, a new study points to another problem: Pregnant women who lived near areas where flaring is common had 50 percent greater odds of giving birth prematurely than those who did not. These births occurred before 37 weeks of gestation, when incomplete development raises a baby’s chance of numerous disorders, even death.

“It’s on par with the increased risk you see for women who smoke,” said Lara Cushing, an assistant professor of environmental health sciences at the University of California, Los Angeles, and lead author of the study. Unlike smoking, however, “it’s not really something you can do much about on an individual level,” she said.

The analysis also found that the impacts of flaring fell entirely on Hispanic mothers, raising concerns about environmental injustice at a time when questions of racial inequality have gripped the nation.

Past research has shown that living near oil and gas wells increases the odds of adverse birth outcomes. The study, published last week in Environmental Health Perspectives, is the first to look specifically at flaring.

Oil and gas producers flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable. Burning the gas prevents methane, a potent greenhouse gas, from escaping to the atmosphere, but it still releases planet-warming carbon dioxide and other harmful chemicals.

Dr. Cushing and her colleagues analyzed satellite images to track nightly flare activity across the Eagle Ford Shale in Texas, which can be seen from space as a crescent of twinkling lights between Laredo and San Antonio. In an earlier study, the researchers counted 43,000 flares between 2012 and 2016.

Over that same period, women in the region gave birth to 23,500 babies. The study found that the odds of preterm birth were 30 percent higher for mothers who lived within three miles of an oil and gas well compared with those who did not, and 50 percent higher for women who were exposed to 10 or more flares over the course of their pregnancies.

It can be hard to tease out cause and effect in retrospective studies such as this, said Dr. Heather Burris, a neonatologist at the University of Pennsylvania’s Perelman School of Medicine who was not involved in the work. But Dr. Burris said the researchers did their best to rule out factors that might make some women prone to preterm birth, like age, smoking habits, socioeconomic status and access to prenatal care.

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The Texas Oil and Gas Association took issue with the study. “The researchers used proximity as a surrogate for exposure,” said Todd Staples, president of the association and a member of the Texas Methane and Flaring Coalition, in a statement. He added that “oil and natural gas companies continue to make great strides in environmental progress.”

Scientists do not know exactly why some women give birth prematurely, Dr. Burris said. But the new study adds to growing evidence that environmental factors play an important role.CLIMATE FWD: What on earth is going on? Get the latest news about climate change, plus tips on how you can help.Sign Up

In the case of flaring, researchers say the mechanism may involve particulate matter, volatile organic compounds and other toxic substances. “It seems pretty plausible that it would have an effect on premature birth given that air pollution and preterm birth are well linked,” said Elaine Hill, a health economist at the University of Rochester Medical Center who was not involved in the study.

The results highlight stark racial disparities in environmental health because the connection between flaring and preterm birth only emerged among Hispanic women, who made up a majority of the study population. Flaring did not increase the risk of preterm birth for non-Hispanic white women, who accounted for about a third of mothers in the study.

Dr. Cushing said there are several potential explanations. On average, Hispanic women experienced more flaring, and it’s possible that the effects only manifest above a certain threshold of exposure. Other studies have also shown that women of color are more susceptible to pollution. That may be because their bodies are already worn down by longtime health problems, exposure to other contaminants or chronic stress caused by discrimination, Dr. Cushing said.

Although the study didn’t address it, economics could also provide part of the answer, Dr. Hill said. If white women in the study were more likely to own land, and thus mineral rights, then the income bumps they received from oil and gas extraction could have offset negative health effects, she said.

Whatever the reason, Dr. Burris said the study suggests that flaring poses a danger to expectant mothers. “I wouldn’t go as far as to say that it’s safe for some women and not others,” she said. “No way.”

Flaring has increased in the U.S. in recent years, but there are efforts to curb the practice. Last week, a federal court blocked the Trump administration’s attempt to roll back Obama-era regulations that discouraged flaring. The Texas Railroad Commission, which oversees the state’s oil and gas industry, is also considering tightening flaring regulations.

Diana Lopez, executive director of the Southwest Workers Union in San Antonio, which advocates for environmental justice, said she hoped the study would bring new urgency to the issue by showing how vulnerable populations bear the collateral costs of fossil fuel extraction.

“That’s just a classic example of environmental racism,” she said.Despite Their Promises, Giant Energy Companies Burn Away Vast Amounts of Natural GasOct. 16, 2019A version of this article appears in print on July 23, 2020, Section A, Page 18 of the New York edition with the headline: New Study Ties Gas Flares To Risk of Premature Birth. Order Reprints | Today’s Paper | Subscribe

August 2020, New York Times

Study Links Gas Flares to Preterm Births, With Hispanic Women at High Risk

Expectant mothers who lived near flaring sites had higher odds of giving birth prematurely than those who did not, researchers found. The adverse outcomes fell entirely on Hispanic women.

A flare in Loving County, Texas. Energy companies flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable.
A flare in Loving County, Texas. Energy companies flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable.Credit…Angus Mordant/Reuters

By Julia Rosen

  • Published July 22, 2020Updated July 23, 2020

Across the United States, gas flares light the night skies over oil and gas fields — visible symbols of the country’s energy boom. They also emit greenhouse gases, making them symbols of climate change that many environmental groups would like to see snuffed out.

Now, a new study points to another problem: Pregnant women who lived near areas where flaring is common had 50 percent greater odds of giving birth prematurely than those who did not. These births occurred before 37 weeks of gestation, when incomplete development raises a baby’s chance of numerous disorders, even death.

“It’s on par with the increased risk you see for women who smoke,” said Lara Cushing, an assistant professor of environmental health sciences at the University of California, Los Angeles, and lead author of the study. Unlike smoking, however, “it’s not really something you can do much about on an individual level,” she said.

The analysis also found that the impacts of flaring fell entirely on Hispanic mothers, raising concerns about environmental injustice at a time when questions of racial inequality have gripped the nation.

Past research has shown that living near oil and gas wells increases the odds of adverse birth outcomes. The study, published last week in Environmental Health Perspectives, is the first to look specifically at flaring.

Oil and gas producers flare natural gas when it is too abundant to capture and sell, or when low prices make doing so unprofitable. Burning the gas prevents methane, a potent greenhouse gas, from escaping to the atmosphere, but it still releases planet-warming carbon dioxide and other harmful chemicals.

Dr. Cushing and her colleagues analyzed satellite images to track nightly flare activity across the Eagle Ford Shale in Texas, which can be seen from space as a crescent of twinkling lights between Laredo and San Antonio. In an earlier study, the researchers counted 43,000 flares between 2012 and 2016.

Over that same period, women in the region gave birth to 23,500 babies. The study found that the odds of preterm birth were 30 percent higher for mothers who lived within three miles of an oil and gas well compared with those who did not, and 50 percent higher for women who were exposed to 10 or more flares over the course of their pregnancies.

It can be hard to tease out cause and effect in retrospective studies such as this, said Dr. Heather Burris, a neonatologist at the University of Pennsylvania’s Perelman School of Medicine who was not involved in the work. But Dr. Burris said the researchers did their best to rule out factors that might make some women prone to preterm birth, like age, smoking habits, socioeconomic status and access to prenatal care.

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The Texas Oil and Gas Association took issue with the study. “The researchers used proximity as a surrogate for exposure,” said Todd Staples, president of the association and a member of the Texas Methane and Flaring Coalition, in a statement. He added that “oil and natural gas companies continue to make great strides in environmental progress.”

Scientists do not know exactly why some women give birth prematurely, Dr. Burris said. But the new study adds to growing evidence that environmental factors play an important role.CLIMATE FWD: What on earth is going on? Get the latest news about climate change, plus tips on how you can help.Sign Up

In the case of flaring, researchers say the mechanism may involve particulate matter, volatile organic compounds and other toxic substances. “It seems pretty plausible that it would have an effect on premature birth given that air pollution and preterm birth are well linked,” said Elaine Hill, a health economist at the University of Rochester Medical Center who was not involved in the study.

The results highlight stark racial disparities in environmental health because the connection between flaring and preterm birth only emerged among Hispanic women, who made up a majority of the study population. Flaring did not increase the risk of preterm birth for non-Hispanic white women, who accounted for about a third of mothers in the study.

Dr. Cushing said there are several potential explanations. On average, Hispanic women experienced more flaring, and it’s possible that the effects only manifest above a certain threshold of exposure. Other studies have also shown that women of color are more susceptible to pollution. That may be because their bodies are already worn down by longtime health problems, exposure to other contaminants or chronic stress caused by discrimination, Dr. Cushing said.

Although the study didn’t address it, economics could also provide part of the answer, Dr. Hill said. If white women in the study were more likely to own land, and thus mineral rights, then the income bumps they received from oil and gas extraction could have offset negative health effects, she said.

Whatever the reason, Dr. Burris said the study suggests that flaring poses a danger to expectant mothers. “I wouldn’t go as far as to say that it’s safe for some women and not others,” she said. “No way.”

Flaring has increased in the U.S. in recent years, but there are efforts to curb the practice. Last week, a federal court blocked the Trump administration’s attempt to roll back Obama-era regulations that discouraged flaring. The Texas Railroad Commission, which oversees the state’s oil and gas industry, is also considering tightening flaring regulations.

Diana Lopez, executive director of the Southwest Workers Union in San Antonio, which advocates for environmental justice, said she hoped the study would bring new urgency to the issue by showing how vulnerable populations bear the collateral costs of fossil fuel extraction.

“That’s just a classic example of environmental racism,” she said.Despite Their Promises, Giant Energy Companies Burn Away Vast Amounts of Natural GasOct. 16, 2019A version of this article appears in print on July 23, 2020, Section A, Page 18 of the New York edition with the headline: New Study Ties Gas Flares To Risk of Premature Birth. Order Reprints | Today’s Paper | Subscribe