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Background <p>Incidence of childhood Ewing sarcoma, a rare cancer affecting bones and soft tissues, is increasing. Environmental exposures during the perinatal period, like air pollution, may play a role. We examined exposure to perinatal ambient fine particulate matter (PM<sub>2.5</sub>) and childhood Ewing sarcoma risk in a case-control linkage study nested within a California birth cohort.</p> Methods <p>The study included 388 children born in California (1982–2015) and diagnosed with Ewing sarcoma at age 0–19 years (1988–2015), and 19,341 California-born cancer-free controls frequency-matched to cases on birth year (50:1 ratio). Ambient PM<sub>2.5</sub> concentrations at the maternal residence were averaged separately over two time periods, gestation and the first year after birth, using a validated ensemble-based model (categorized as quartiles). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) for the association between perinatal PM<sub>2.5</sub> exposure and Ewing sarcoma risk, adjusting for sex, birth year, race, ethnicity, birth weight, and maternal education and stratifying by Hispanic ethnicity to assess potential disparities in PM<sub>2.5</sub>-related cancer risk.</p> Results <p>In the overall population, perinatal ambient PM<sub>2.5</sub> exposure was not associated with Ewing sarcoma risk when considering exposure during gestation or the year after birth. Among Hispanic children, who experienced greater air pollution exposure compared to non-Hispanic children, higher PM<sub>2.5</sub> levels during gestation yielded elevated odds of Ewing sarcoma compared to the first quartile (Q2 OR [95% CI] = 1.53 [0.94–2.51]; Q3 = 1.56 [0.95–2.56]; Q4 = 1.39 [0.79–2.47]). Hispanic children also experienced elevated risk in relation to exposure during the year after birth.</p> Conclusion <p>Our results provide new suggestive evidence that ambient PM<sub>2.5</sub> may contribute to Ewing sarcoma risk, although these findings were not statistically significant and were specific to Hispanic children. These findings require replication and underscore the need to further evaluate the potential role of ethnicity in the PM<sub>2.5</sub>-cancer relationship with genetic ancestry measures and through the lens of environmental justice.</p>

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Perinatal exposure to ambient fine particle air pollution and risk of childhood ewing sarcoma in a population-based case-control study in California (1988–2015)

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  • 发表日期：

    2025年3月7日

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  • Cassandra J. Clark,
  • Rong Wang,
  • Joseph L. Wiemels,
  • Catherine Metayer,
  • Nicole C. Deziel,
  • Xiaomei Ma

摘要

Background

Incidence of childhood Ewing sarcoma, a rare cancer affecting bones and soft tissues, is increasing. Environmental exposures during the perinatal period, like air pollution, may play a role. We examined exposure to perinatal ambient fine particulate matter (PM2.5) and childhood Ewing sarcoma risk in a case-control linkage study nested within a California birth cohort.

Methods

The study included 388 children born in California (1982–2015) and diagnosed with Ewing sarcoma at age 0–19 years (1988–2015), and 19,341 California-born cancer-free controls frequency-matched to cases on birth year (50:1 ratio). Ambient PM2.5 concentrations at the maternal residence were averaged separately over two time periods, gestation and the first year after birth, using a validated ensemble-based model (categorized as quartiles). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) for the association between perinatal PM2.5 exposure and Ewing sarcoma risk, adjusting for sex, birth year, race, ethnicity, birth weight, and maternal education and stratifying by Hispanic ethnicity to assess potential disparities in PM2.5-related cancer risk.

Results

In the overall population, perinatal ambient PM2.5 exposure was not associated with Ewing sarcoma risk when considering exposure during gestation or the year after birth. Among Hispanic children, who experienced greater air pollution exposure compared to non-Hispanic children, higher PM2.5 levels during gestation yielded elevated odds of Ewing sarcoma compared to the first quartile (Q2 OR [95% CI] = 1.53 [0.94–2.51]; Q3 = 1.56 [0.95–2.56]; Q4 = 1.39 [0.79–2.47]). Hispanic children also experienced elevated risk in relation to exposure during the year after birth.

Conclusion

Our results provide new suggestive evidence that ambient PM2.5 may contribute to Ewing sarcoma risk, although these findings were not statistically significant and were specific to Hispanic children. These findings require replication and underscore the need to further evaluate the potential role of ethnicity in the PM2.5-cancer relationship with genetic ancestry measures and through the lens of environmental justice.