Background:

Environmental cadmium exposure is widespread. In humans, cadmium is poorly excreted, triggers pulmonary inflammation, reduces pulmonary function, and enhances lung injury by respiratory syncytial virus.

Objectives:

We examined the association of cadmium burden with mortality related to influenza or pneumonia.

Methods:

This prospective analysis of the National Health and Nutrition Examination Survey (NHANES) included 7,173 and 8,678 participants ≥45 years of age enrolled in NHANES-III and NHANES 1999–2006, respectively. Associations were evaluated between cadmium and mortality from influenza or pneumonia during a median follow-up of 17.3 y (NHANES-III, based on creatinine-corrected urine cadmium) and 11.4 y (NHANES 1999–2006, based on blood cadmium). Survey-weighted Cox proportional hazard models were used to compute hazard ratios (HRs) comparing the mortality of individuals at the 80th vs. the 20th percentile of cadmium concentrations.

Results:

In NHANES-III, after adjustment for sex, race/ethnicity, education, body mass index, serum cholesterol, hypertension, and NHANES phase (or cycle), the HR comparing influenza or pneumonia mortality among participants with creatinine-corrected urinary cadmium in the 80th vs. 20th percentile was 1.15 (95% CI: 1.05, 1.26; p=0.002) in the population as a whole and 1.27 (95% CI: 1.12, 1.43; p=0.002) among never smokers. In NHANES 1999–2006, adjusted HRs for the 80th vs. 20th percentile of blood cadmium were 1.14 (95% CI: 0.96, 1.36; p=0.15) for the overall population and 1.71 (95% CI: 0.95, 3.09; p=0.07) in never smokers.

Discussion:

Among middle-aged and older adults in the United States, higher cadmium burdens are associated with higher mortality from influenza or pneumonia. This raises the possibility that cadmium may worsen outcomes from COVID-19 infections. https://doi.org/10.1289/EHP7598

Human controlled exposure studies suggest that diesel exhaust causes acute changes in blood pressure that are mediated by sympathetic activation, but it is unknown whether this sympathetic response might also cause imbalance directly affecting cardiac autonomic control. Baroreceptor sensitivity (BRS) measures rapid compensatory regulation of heart rate in response to acute changes in blood pressure. Using a crossover trial of real-world in-vehicle commutes, we tested whether exposure to traffic-related air pollutants (TRAP) affects spontaneous BRS in healthy subjects.Young healthy participants were driven through heavy Seattle, WA traffic for two hours on three different days, each separated by several weeks. On two days, on-road air was entrained into the cabin through the vehicle’s factory air vents and sham filters. On another day, the vehicle was equipped with effective filtration. Exposure was double-blinded and participants were randomized to order of exposure. Three minute intervals of continuous blood pressure and pulse intervals were recorded before, during, and up to 24 hours after drive using a Finapres finger pulse waveform device. BRS was calculated as the reduced major axis slope for change in pulse interval per change in blood pressure for rolling 10 second intervals.On filtered days in-vehicle average particle count was reduced by 85%. We used a mixed effects model on the outcome of change from pre-drive BRS measurements, comparing filtered versus unfiltered day at all thirteen time points in nine subjects with measurable BRS, after excluding a single subject with very large changes in BRS. A likelihood ratio test for the effect of filtration on BRS at all time points was not significant (p=0.95). At 7 hours after drive start, BRS, relative to pre-drive levels, was on average 1.01 ms/mmHg higher (95% CI:-7.4, 9.4) in unfiltered drives compared to filtered drives. In conclusion, we did not find evidence that TRAP inhalation causes acute change in BRS.