J Dairy Sci. 2022 Jun 15:S0022-0302(22)00345-9. doi: 10.3168/jds.2022-22135. Online ahead of print.
Wildfires are particularly prevalent in the Western United States, home to more than 2 million dairy cows that produce more than 25% of the nation’s milk. Wildfires emit fine particulate matter (PM2.5) in smoke, which is a known air toxin and is thought to contribute to morbidity in humans by inducing inflammation. The physiological responses of dairy cows to wildfire PM2.5 are unknown. Herein we assessed the immune, metabolic, and production responses of lactating Holstein cows to wildfire PM2.5 inhalation. Cows (primiparous, n = 7; multiparous, n = 6) were monitored across the wildfire season from July to September 2020. Cows were housed in freestall pens and thus were exposed to ambient air quality. Air temperature, relative humidity, and PM2.5 were obtained from a monitoring station 5.7 km from the farm. Animals were considered to be exposed to wildfire PM2.5 if daily average PM2.5 exceeded 35 µg/m3 and wildfire and wind trajectory mapping showed that the PM2.5 derived from active wildfires. Based on these conditions, cows were exposed to wildfire PM2.5 for 7 consecutive days in mid-September. Milk yield was recorded daily and milk components analysis conducted before, during, and after exposure. Blood was taken from the jugular vein before, during, and after exposure and assayed for hematology, blood chemistry, and blood metabolites. Statistical analysis was conducted using mixed models including PM2.5, temperature-humidity index (THI), parity (primiparous or multiparous), and their interactions as fixed effects and cow as a random effect. Separate models included lags up to 7 d to identify delayed and persistent effects from wildfire PM2.5 exposure. Exposure to elevated PM2.5 from wildfire smoke resulted in lower milk yield during exposure and for 7 d after last exposure and higher blood CO2 concentration, which persisted for 1 d following exposure. We observed a positive PM2.5 by THI interaction for eosinophil and basophil count and a negative PM2.5 by THI interaction for red blood cell count and hemoglobin concentration after a 3-d lag. Neutrophil count was also lower with a combination of higher THI and PM2.5. We found no discernable effect of PM2.5 on haptoglobin concentration. Effects of PM2.5 and THI on metabolism were contingent on day of exposure. On lag d 0, blood urea nitrogen (BUN) was reduced with higher combined THI and PM2.5, but on subsequent lag days, THI and PM2.5 had a positive interaction on BUN. Conversely, THI and PM2.5 had a positive interacting effect on nonesterified fatty acids (NEFA) on lag d 0 but subsequently caused a reduction in circulating NEFA concentration. Our results suggest that exposure to high wildfire-derived PM2.5, alone or in concert with elevated THI, alters systemic metabolism, milk production, and the innate immune system.