Beyond ozone, there is a growing public health concern over fine particulate matter (PM2.5)—airborne particles small enough to be inhaled deep into the lungs. A key strategic insight for policymakers is that actions designed to reduce photochemical smog can serve as a force multiplier for public health by also reducing these harmful particles. A significant fraction of urban PM2.5 is not emitted directly but is formed in the atmosphere.

These particles are known as Secondary Organic Aerosols (SOAs). They are formed when low-volatility products from the photooxidation of hydrocarbons—primarily VOCs—condense from a gas into a solid or liquid particulate phase.

Crucially, the very same chemical processes that drive ozone formation are also responsible for creating the precursor gases for SOAs. The hydroxyl radical (OH)-initiated oxidation of VOCs from sources like simulated auto exhaust (Kleindienst et al., 2002) and naturally occurring biogenic hydrocarbons (Griffin et al., 1999) generates the low-vapor-pressure compounds that ultimately become particulate matter. Therefore, policies aimed at controlling VOCs to reduce ozone simultaneously cut the raw material needed for SOA formation.

This link holds true even for VOCs with low particulate yields. For example, while isoprene—a biogenic VOC emitted in massive quantities by vegetation—has a low aerosol yield on its own, its immense global emission quantities mean it can still be a significant source of SOAs globally. Larger biogenic hydrocarbons, which are also abundant, are expected to have much higher SOA yields, reinforcing the connection.

Controlling VOC emissions is therefore a dual-impact strategy. It directly addresses the formation of photochemical smog while simultaneously disrupting the atmospheric production of harmful secondary particulate matter, delivering a critical public health dividend.