Artificial light at night is among the most pervasive forms of environmental change on Earth. More than 80 percent of the human population now lives under light-polluted skies, and that figure grows by a few percent each year. Research over the past decade has documented disruptions to the biology of birds, insects, bats, sea turtles and flowering plants, most of them traceable to artificial light that is scrambling the circadian and photoperiodic systems that organisms use to coordinate their behavior, physiology and timing with the rest of the natural world.

A new study in the Journal of Applied Ecology asks what city lights do to the autumn dormancy of the northern house mosquito, Culex pipiens , the primary vector of West Nile virus in cities across the northeastern and midwestern United States. The answer is that dim residential lighting, at intensities typical of a porch light, suppresses mosquito dormancy more powerfully than even urban warming does. Mosquitoes that should be sleeping in October are still biting, still blood-feeding, still producing eggs.

Each autumn, as day length shortens, female Culex pipiens enter diapause: a state of developmental arrest in which they stop seeking hosts, halt egg development, accumulate fat reserves, and seek sheltered hibernation sites. While dormant, they cannot transmit pathogens. The predictable decline of West Nile virus cases in October across the northern United States reflects this shutdown.

The shutdown is triggered primarily by photoperiod, not temperature. Daylength is one of the most reliable environmental cues available to an organism. October 15 has almost the same amount of daylight every year, regardless of weather. Temperature is far more variable: a warm November can follow a cold October, and an insect that relied on temperature to predict winter would sometimes be badly wrong. The evolutionary solution, for most temperate insects, is to use the light signal as the primary trigger and treat temperature as a secondary modifier.

City lights falsify that signal. A mosquito larva reared under a porch light cannot distinguish it from an abnormally long day. It behaves accordingly, deferring dormancy, developing reproductively, remaining active.

Researchers from Ohio State University tested this directly, in conditions close to real urban life. Over two autumn seasons, they reared Culex pipiens larvae in enclosures placed at residential, school, and church properties across Columbus, Ohio. Each property hosted two enclosures: one positioned near an existing outdoor light source, the other in a dark location on the same site.

The lights were whatever the property owners already had: porch fixtures, garage lights, garden path lights. Mean illumination inside the lit enclosures was roughly five lux, with some sites below one lux.

The September results were striking for what they revealed about the two signals competing to control dormancy. In dark enclosures, warmer nights reduced diapause incidence, exactly as expected: temperature was doing its usual work. In light-exposed enclosures, temperature had no detectable effect on diapause at all. The light signal had fully overridden the thermal one.

October was more extreme. Every mosquito in dark enclosures entered diapause. Among light-exposed mosquitoes, roughly 59 percent still did, but 41 percent did not. Of those that remained active, a substantial fraction took a blood meal when brought to the laboratory and offered one, and went on to produce hatching offspring.

Why Light Dominates Temperature

Cities disrupt both signals simultaneously. The Urban Heat Island effect raises nighttime temperatures, and urban warming has been a focus of research on extended mosquito seasons precisely because it is measurable and has intuitive biological plausibility. The new study does not dismiss that effect; it shows that urban warming does delay dormancy onset, at least in the early autumn. What it also shows is that light pollution is the stronger driver, and that when both disturbances are present, the light signal governs.

Temperature has been a variable feature of the environment across insect evolutionary history: populations have experienced warm autumns and cold autumns and have therefore developed phenotypic plasticity, the capacity to adjust their biology in response to varying conditions, with respect to temperature. Light-dark cycles, by contrast, have been essentially fixed for hundreds of millions of years. The genetic machinery for responding to photoperiod is deeply conserved; there is no evolutionary precedent for light at the wrong time of night, and therefore no adaptive buffer against it.

Moths, flesh flies, tiger mosquitoes and several passerine bird species show the same pattern: when artificial light falsifies the photoperiod signal, they behave as though it is still summer. What the Ohio State study adds is a direct comparison with urban warming in the same experiment, and a demonstration that even at the low intensities characteristic of ordinary residential lighting, light pollution wins.

Implications for Disease Transmission

Extending the season during which Culex pipiens is active and feeding is one mechanism by which city lights could elevate disease risk. But it is not the only one.

House sparrows, common urban reservoir hosts for West Nile virus, remain infectious to biting mosquitoes for approximately two days longer when exposed to artificial light at night, compared to birds in natural light conditions. A 2019 study traced this to circadian disruption of immune gene regulation: light-exposed birds mounted antiviral responses earlier, but cleared the virus less effectively, maintaining transmissible viral loads into a period when control birds had already recovered. The mathematical implication, given reasonable parameter values, was a substantial increase in outbreak potential.

A 2021 analysis of West Nile surveillance data from five Florida counties found that artificial light at night was a stronger predictor of exposure risk in sentinel chickens than impervious surface cover, population density, or the human footprint index, standard urbanization variables that epidemiologists examine.

These three lines of evidence describe a system in which city lights operate on both sides of the transmission cycle: vectors remain active later and reservoir hosts remain infectious longer. Those effects have not been modeled jointly, and what they add to existing estimates of urban disease risk is unknown.