links between cooking aerosols exposure and acute cardiopulmonary and neurological responses: A clinical investigation

Abstract

Indoor air quality is a growing public health concern, particularly due to the increasing time individuals spend indoors, where they are exposed to a variety of aerosols and pollutants generated by everyday household activities. The prevalence of cooking as a daily activity has raised significant concerns regarding the associated health impacts of cooking aerosols, particularly ultrafine particles (UFPs) and particulate matter (PM) emissions. These pollutants can penetrate deep into the lungs and bloodstream, potentially causing adverse cardiovascular, respiratory, and neurological health effects. The complex composition of cooking aerosols varies significantly depending on the type of stove used, the cooking methods employed, and the specific food items prepared. For instance, frying and grilling are known to produce higher concentrations of UFPs compared to boiling or steaming. Furthermore, the combustion process can generate not only particulate matter but also a variety of gaseous pollutants, including nitrogen dioxide (NO2) and carbon monoxide (CO), which can further exacerbate health risks. Despite the well-documented risks associated with solid fuel cooking, there is a lack of controlled human exposure studies on the health impacts of gas and electric stove emissions. In this study, we present a new exposure design that addresses several key shortcomings in prior human exposure studies. By carrying out tightly controlled exposure sessions, we reduced the risk of confounding by post-exposure environments, especially in the essential time frame leading up to a 24-hour follow-up measure and exposure during commuting. To our knowledge, this is the first time that the particulate and gaseous fractions of cooking emission effects on cardiopulmonary outcomes have been isolated in a comprehensive manner, enabling a finer estimate of their individual adverse impacts on health. In this study, we introduce a unique intervention method using P100 respirators to isolate the effects of particles and gases, decoupling their respective contributions to health outcomes. Furthermore, this is the first study to measure acute cognitive function responses to gaseous components of cooking air pollution, which is a long-standing gap in the scientific literature. The research presented in this thesis was aimed at addressing these gaps by investigating the health effects of cooking aerosols from gas and electric stoves, post short-term (30 minutes and 2 hours) and medium-term (24-hour) exposure. A series of controlled human exposure studies were conducted, employing novel methodologies to assess cardiopulmonary and neurological responses while accounting for exposure to different particle sizes and gaseous pollutants. To achieve this, a cohort of healthy adult participants was recruited for controlled exposure studies, where they were subjected to cooking emissions in a monitored environment. Using a novel exposure setup, healthy adults were exposed to emissions under controlled conditions while minimizing post-exposure confounding. A unique intervention using P100 respirators was employed to decouple particle and gas effects. This investigation employed a range of assessment techniques, including cognitive tests to evaluate neurocognitive responses, as well as measurements of blood pressure, electrocardiogram (ECG), fractional exhaled nitric oxide (FeNO), and peak flow meter readings to assess cardiopulmonary effects. The findings reveal that cooking generates significant amounts of UFPs, which have immediate and sustained impacts on lung and heart function. Analysis of the data indicated that cooking-generated aerosols—comprising both particles and gases—had no statistically significant impact on PEFR, SBP, HR, or SpO₂ up to 24 hours post-exposure; however, significant effects were observed for FeNO and DBP, indicating inflammatory and vascular responses. A significant 9.35 % decrease in DBP was observed immediately after cooking, while FeNO rose by 73.24 % right after cooking and remained 60.27 % higher 30 minutes later. The gas-only exposure intervention (from electric stove emissions) revealed no significant changes in DBP, SBP, HR, SpO₂, or PEFR, yet cognitive assessments suggested a transient disruption in memory and attention, likely due to neurocognitive distraction caused by cooking-related gases. These findings underscore the dominant role of particulate matter—rather than gaseous by-products—in driving acute physiological responses to cooking emissions, highlighting the need for targeted mitigation strategies to reduce indoor particle exposure during cooking activities. This research provides valuable insights into how cooking-related pollutants affect human health and offers recommendations for future studies to enhance understanding and policy development in this critical area of public health.