The world is undergoing massive atmospheric and ecological change, driving unprecedented challenges to human well-being. Olfaction is a key sensory system through which these impacts occur. The sense of smell influences quality of and satisfaction with life, emotion, emotion regulation, cognitive function, social interactions, dietary choices, stress, and depressive symptoms. Exposures via the olfactory pathway can also lead to (anti-)inflammatory outcomes. Increased understanding is needed regarding the ways in which odorants generated by nature (i.e., natural olfactory environments) affect human well-being. With perspectives from a range of health, social, and natural sciences, we provide an overview of this unique sensory system, four consensus statements regarding olfaction and the environment, and a conceptual framework that integrates the olfactory pathway into an understanding of the effects of natural environments on human well-being. We then discuss how this framework can contribute to better accounting of the impacts of policy and land-use decision-making on natural olfactory environments and, in turn, on planetary health.

Background: Numerous epidemiological studies indicated high levels of particulate matter less than2.5 μm diameter (PM_2.5) as a major cardiovascular risk factor. Most of the studies have been conducted in high-income countries (HICs), where average levels of PM_2.5 are far less compared to low- and middle- income countries (LMICs), and their socio-economic profile, disease burden, and PM speciation/composition are very different. We systematically reviewed the association of long-term exposure to PM_2.5 and cardio-metabolic diseases (CMDs) in LMICs. Methods: Multiple databases were searched for English articles with date limits until March 2018. We included studies investigating the association of long-term exposure to PM_2.5 (defined as an annual average/average measure for 3 more days of PM_2.5 exposure) and CMDs, such as hospital admissions, prevalence, and deaths due to CMDs, conducted in LMICs as defined by World Bank. We excluded studies which employed exposure proxy measures, studies among specific occupational groups, and specific episodes of air pollution. Results: A total of 5567 unique articles were identified, of which only 17 articles were included for final review, and these studies were from Brazil, Bulgaria, China, India, and Mexico. Outcome assessed were hypertension, type 2 diabetes mellitus and insulin resistance, and cardiovascular disease (CVD)-related emergency room visits/admissions, death, and mortality. Largely a positive association between exposure to PM_2.5 and CMDs was found, and CVD mortality with effect estimates ranging from 0.24% to 6.11% increased per 10 μg/m³ in PM_2.5. CVD-related hospitalizations and emergency room visits increased by 0.3% to 19.6%. Risk factors like hypertension had an odds ratio of 1.14, and type 2 diabetes mellitus had an odds ratio ranging from 1.14–1.32. Diversity of exposure assessment and health outcomes limited the ability to perform a meta-analysis. Conclusion: Limited evidence on the association of long-term exposure to PM_2.5 and CMDs in the LMICs context warrants cohort studies to establish the association.

Ozone (O₃), a major component of urban air pollution, is a strong oxidizing agent that can cause lung injury and inflammation. In the present study, we investigated the effect of inhalation of O₃ on levels of F₂-isoprostanes in bronchoalveolar lavage fluid (BALF) and on levels of antioxidants in the BALF and plasma of hamsters. Because antioxidants, including urate, ascorbate, GSH, and vitamin E, defend the lungs by reacting with oxidizing agents, we expected to find a decrease in antioxidant levels after O₃exposure. Similarly, we expected an increase in the levels of F₂-isoprostanes, which are lipid peroxidation products. Exposure to 1.0 or 3.0 parts/million (ppm) O₃ for 6 h resulted in an increase in BALF neutrophil numbers, an indicator of acute inflammation, as well as elevation of BALF F₂-isoprostanes. The higher dose of O₃ caused an increase in the BALF level of urate and a decrease in the plasma level of ascorbate, but 1.0 ppm O₃ had no effect on BALF or plasma antioxidant levels. Exposure to 0.12 ppm O₃ had no effect on BALF neutrophils or F₂-isoprostanes nor on BALF and plasma antioxidants. We also investigated the effect of O₃ exposure of hamsters during exercise on F₂-isoprostane and antioxidant levels. We found that exposure to 1.0 ppm O₃ during 1 h of exercise on a laddermill increased BALF levels of F₂-isoprostanes but had no effect on BALF neutrophils or on BALF and plasma antioxidants. These results indicate that O₃ induces inflammation and biomolecule oxidation in the lungs, whereas extracellular antioxidant levels are relatively unchanged.

Introduction: Air pollution presents a major public health threat to India, affecting more than three quarters of the country’s population. In the current project, GEOHealth Health Effects of Selected Environmental Exposomes Across the Life CourSe–India, we aim to study the effect of environmental exposomes—fine particulate matter (PM _2.5 ), nitrogen dioxide (NO ₂ ), ozone (O ₃ ) and extremes of temperature—on multiple health outcomes using a modified life course approach. The associated training grant aims to build capacity in India to address the unique environmental health problems. Methods and analysis: The project aims to (A) Develop exposure assessments in seven cities, namely Delhi, Chennai, Sonipat, Vizag, Pune, Hyderabad and Bikaner, for: (1) A fine-scale spatiotemporal model for multiple pollutants (PM _2.5 , NO ₂ , O _3, temperature); (2) Combined ground monitoring and modelling for major chemical species of ambient PM _2.5 at seven cities; and (3) Personal exposure assessment in a subsample from the six cities, except Pune, and (B) Conduct health association studies covering a range of chronic non-communicable diseases and their risk factors leveraging a unique approach using interdigitating cohorts. We have assembled existing pregnancy, child, adolescent, adult and older adult cohorts across India to explore health effects of exposomes using causal analyses. We propose to use Bayesian kernel machine regression to assess the effects of mixtures of all pollutants including species of PM _2.5 on health while accounting for potential non-linearities and interactions between exposures. This builds on earlier work that constructed a fine spatiotemporal model for PM _2.5 exposure to study health outcomes in two Indian cities. Ethics and dissemination: Ethical clearance for conduct of the study was obtained from the Institutional Ethics Committee (IEC) of the Centre for Chronic Disease Control, and all the participating institutes and organisations. National-level permission was provided by the Indian Council of Medical Research. The research findings will be disseminated through peer-reviewed publications, policy briefs, print and social media, and communicating with the participating communities and stakeholders. Training of Indian scientists will build the capacity to undertake research on selected adverse environmental exposures on population health in India.