PDF(Pubmed)
Abstract：
Racial/ethnic disparities in hypertension are a pressing public health problem. The contribution of environmental pollutants including PFAS have not been explored, even though certain PFAS are higher in Black population and have been associated with hypertension.
We examined the extent to which racial/ethnic disparities in incident hypertension are explained by racial/ethnic differences in serum PFAS concentrations.
We included 1058 hypertension-free midlife women with serum PFAS concentrations in 1999-2000 from the multi-racial/ethnic Study of Women\'s Health Across the Nation with approximately annual follow-up visits through 2017. Causal mediation analysis was conducted using accelerated failure time models. Quantile-based g-computation was used to evaluate the joint effects of PFAS mixtures.
During 11,722 person-years of follow-up, 470 participants developed incident hypertension (40.1 cases per 1000 person-years). Black participants had higher risks of developing hypertension (relative survival: 0.58, 95% CI: 0.45-0.76) compared with White participants, which suggests racial/ethnic disparities in the timing of hypertension onset. The percent of this difference in timing that was mediated by PFAS was 8.2% (95% CI: 0.7-15.3) for PFOS, 6.9% (95% CI: 0.2-13.8) for EtFOSAA, 12.7% (95% CI: 1.4-22.6) for MeFOSAA, and 19.1% (95% CI: 4.2, 29.0) for PFAS mixtures. The percentage of the disparities in hypertension between Black versus White women that could have been eliminated if everyone\'s PFAS concentrations were dropped to the 10th percentiles observed in this population was 10.2% (95% CI: 0.9-18.6) for PFOS, 7.5% (95% CI: 0.2-14.9) for EtFOSAA, and 17.5% (95% CI: 2.1-29.8) for MeFOSAA.
These findings suggest differences in PFAS exposure may be an unrecognized modifiable risk factor that partially accounts for racial/ethnic disparities in timing of hypertension onset among midlife women. The study calls for public policies aimed at reducing PFAS exposures that could contribute to reductions in racial/ethnic disparities in hypertension.
We examined the extent to which racial/ethnic disparities in incident hypertension are explained by racial/ethnic differences in serum PFAS concentrations.
We included 1058 hypertension-free midlife women with serum PFAS concentrations in 1999-2000 from the multi-racial/ethnic Study of Women\'s Health Across the Nation with approximately annual follow-up visits through 2017. Causal mediation analysis was conducted using accelerated failure time models. Quantile-based g-computation was used to evaluate the joint effects of PFAS mixtures.
During 11,722 person-years of follow-up, 470 participants developed incident hypertension (40.1 cases per 1000 person-years). Black participants had higher risks of developing hypertension (relative survival: 0.58, 95% CI: 0.45-0.76) compared with White participants, which suggests racial/ethnic disparities in the timing of hypertension onset. The percent of this difference in timing that was mediated by PFAS was 8.2% (95% CI: 0.7-15.3) for PFOS, 6.9% (95% CI: 0.2-13.8) for EtFOSAA, 12.7% (95% CI: 1.4-22.6) for MeFOSAA, and 19.1% (95% CI: 4.2, 29.0) for PFAS mixtures. The percentage of the disparities in hypertension between Black versus White women that could have been eliminated if everyone\'s PFAS concentrations were dropped to the 10th percentiles observed in this population was 10.2% (95% CI: 0.9-18.6) for PFOS, 7.5% (95% CI: 0.2-14.9) for EtFOSAA, and 17.5% (95% CI: 2.1-29.8) for MeFOSAA.
These findings suggest differences in PFAS exposure may be an unrecognized modifiable risk factor that partially accounts for racial/ethnic disparities in timing of hypertension onset among midlife women. The study calls for public policies aimed at reducing PFAS exposures that could contribute to reductions in racial/ethnic disparities in hypertension.
摘要：
背景：高血压的种族/民族差异是一个紧迫的公共卫生问题。尚未探索包括PFAS在内的环境污染物的贡献，尽管某些PFAS在黑人人群中较高，并且与高血压有关。
目的：我们研究了因血清PFAS浓度的种族/民族差异来解释高血压的种族/民族差异的程度。
方法：我们在1999-2000年纳入了1058名无高血压的中年女性，他们的血清PFAS浓度来自全国妇女健康的多种族/民族研究，大约每年随访一次，直到2017年。使用加速故障时间模型进行因果中介分析。基于分位数的g计算用于评估PFAS混合物的联合作用。
结果：在11,722人年的随访中，470名参与者发生高血压（每1000人年40.1例）。与白人参与者相比，黑人参与者患高血压的风险更高（相对生存率：0.58，95％CI：0.45-0.76）。这表明高血压发病时间的种族/族裔差异。PFAS介导的时间差异百分比为PFOS的8.2％（95％CI：0.7-15.3），EtFOSAA为6.9%（95%CI：0.2-13.8），MeFOSAA的12.7%（95%CI：1.4-22.6），和19.1%(95%CI:4.2,29.0)的PFAS混合物。如果每个人的PFAS浓度下降到该人群中观察到的第10百分位数，则黑人与白人女性之间的高血压差异百分比为PFOS的10.2％（95％CI：0.9-18.6）。EtFOSAA为7.5%（95%CI：0.2-14.9），MeFOSAA占17.5%（95%CI：2.1-29.8）。
结论：这些研究结果表明，PFAS暴露的差异可能是一个无法识别的可改变的危险因素，部分原因是中年女性高血压发病时间的种族/民族差异。该研究呼吁采取旨在减少PFAS暴露的公共政策，这可能有助于减少高血压的种族/族裔差异。
目的：我们研究了因血清PFAS浓度的种族/民族差异来解释高血压的种族/民族差异的程度。
方法：我们在1999-2000年纳入了1058名无高血压的中年女性，他们的血清PFAS浓度来自全国妇女健康的多种族/民族研究，大约每年随访一次，直到2017年。使用加速故障时间模型进行因果中介分析。基于分位数的g计算用于评估PFAS混合物的联合作用。
结果：在11,722人年的随访中，470名参与者发生高血压（每1000人年40.1例）。与白人参与者相比，黑人参与者患高血压的风险更高（相对生存率：0.58，95％CI：0.45-0.76）。这表明高血压发病时间的种族/族裔差异。PFAS介导的时间差异百分比为PFOS的8.2％（95％CI：0.7-15.3），EtFOSAA为6.9%（95%CI：0.2-13.8），MeFOSAA的12.7%（95%CI：1.4-22.6），和19.1%(95%CI:4.2,29.0)的PFAS混合物。如果每个人的PFAS浓度下降到该人群中观察到的第10百分位数，则黑人与白人女性之间的高血压差异百分比为PFOS的10.2％（95％CI：0.9-18.6）。EtFOSAA为7.5%（95%CI：0.2-14.9），MeFOSAA占17.5%（95%CI：2.1-29.8）。
结论：这些研究结果表明，PFAS暴露的差异可能是一个无法识别的可改变的危险因素，部分原因是中年女性高血压发病时间的种族/民族差异。该研究呼吁采取旨在减少PFAS暴露的公共政策，这可能有助于减少高血压的种族/族裔差异。
