For nearly sixty years, the Autism Research Institute (ARI) has tried to understand autism by looking beyond surface behaviors and asking deeper biological questions. From the beginning, Bernard Rimland challenged the dominant view of autism as a purely psychological condition and argued that biology mattered (Rimland, 1964). That position was not widely accepted at the time, but history has proven it correct. Over the years, ARI expanded this biological focus to include genetics, nutrition, immune function, metabolism, and environmental exposures (Edelson, 2017, 2025a). The consistent message has been that autism does not arise from a single contributor, but from the interaction of multiple biological systems with the environment.

One of the lessons learned over decades of research is that some of the most important influences are also the easiest to miss. They are small, commonplace, and part of everyday life. In a previous editorial, Invisible Threats: The Role of Environmental Toxins in Autism, I discussed how environmental exposures often remain underappreciated precisely because they are so familiar (Edelson, 2025b). Air pollution falls squarely into this category.

ARI began paying attention to environmental factors long before large population studies were available. Early on, Rimland, Sidney Baker, Jon Pangborn, and others noticed patterns in parent reports and clinical observations that pointed toward immune dysregulation, metabolic burden, and environmental toxic load. These early efforts were not definitive, but they were consistent. Over time, many of the questions raised in those early years have become the subject of formal epidemiological and biological research (Goodrich et al., 2024; Masi et al., 2017; Oliveira et al., 2005).

In this editorial, I focus on particulate matter, commonly referred to as PM. Particulate matter is a mixture of solid particles and liquid droplets, much of it produced by vehicle exhaust and other combustion sources. These particles range widely in size. Larger particles are heavy enough to fall out of the air within seconds or minutes and deposit on surfaces or in the upper airways. Smaller particles, including PM_2.5 and ultrafine particles (<2.5), can remain suspended for hours or days and travel long distances.

Most people think of air pollution only when it is visible, as haze or smog on certain days. But particulate matter is present even when the air appears clear. It settles on cars and sidewalks, and more importantly, it is inhaled continuously. Exposure is not occasional. It is daily, and for many people, unavoidable.

Because this exposure is constant and its effects are not immediately obvious, PM is often dismissed as background noise. Yet decades of research have established its role in heart and lung disease (see review Hamanaka & Mutlu, 2018). Only more recently has attention turned to its possible effects on other conditions (see review Brockmeyer & D’Angiulli, 2016).

A growing number of studies from different countries now show associations between air pollution exposure and increased likelihood of increased brain-related disorders such as autism, Alzheimer’s disease, and dementia, particularly when exposure occurs before birth or early in life. From an ARI perspective, this trajectory is familiar. Initial observations raise concerns. Early studies provide signals. Over time, evidence accumulates across disciplines. That is exactly what has happened with particulate matter.

How PM enters the body

Two factors are especially important: particle size and toxicity. Particle size affects how easily particulate matter enters the body and reaches organs such as the lungs, cardiovascular system, and brain. Toxicity depends on chemical composition, and particles of the same size can produce very different immune and long-term biological effects. Ultrafine particles, produced largely by vehicle exhaust, particularly diesel emissions, are generally the most chemically reactive and inflammatory. Larger particles from sources such as wildfires and industrial emissions are typically less reactive but can still be harmful with chronic exposure.

Several studies have examined how fine particulate matter may affect the central nervous system (Ishihara et a., 2025). Although air pollution has long been associated with respiratory and cardiovascular conditions, increasing attention is now being directed toward its potential neurological effects. Toxic components such as metals, microplastics, and organic compounds can, under certain conditions, move beyond the lungs and enter systemic circulation. Ultrafine particles may also reach the brain directly through the olfactory pathway or indirectly by influencing the integrity of the blood-brain barrier.

Experimental and epidemiological findings suggest that chronic exposure is associated with neuroinflammation, oxidative stress, and altered neural function. Over time, these biological responses have been linked in population studies to a higher likelihood of neurological conditions, including autism, Alzheimer’s disease, and dementia. Clarifying the specific biological pathways involved remains essential for understanding how environmental exposures may influence brain development and long-term neurological health.

Particulate matter is often treated as a single exposure, but it is not. The same PM level can reflect very different mixtures depending on the source, such as traffic, wildfire smoke, industrial combustion, or even suspended dust. These differences matter because chemical composition strongly influences biological impact. Combustion-related and ultrafine particles are generally more chemically reactive, more inflammatory, and more likely to carry toxic compounds on their surfaces.

Over the past decade, gene expression profiling studies have helped clarify how PM affects biological systems. Despite differences in exposure conditions and PM sources, studies consistently report alterations in pathways involved in detoxification, inflammation, and oxidative stress. Findings from both animal and human exposure studies show similar patterns (Huang, 2013). Together, this evidence indicates that PM exposure can trigger coordinated changes in gene expression that influence immune and metabolic pathways.

PM and autism

Reports of altered detoxification pathways, chronic inflammation, and oxidative stress are not new to autism research. For decades, ARI has monitored patterns of immune activation and metabolic imbalance as a recurring theme. What is emerging more clearly now is the recognition that common environmental exposures may interact with these biological systems during critical windows of development, potentially amplifying underlying vulnerabilities (Ishihara et al., 2025; Jung et al., 2024; Wang et al., 2024).

In recent years, numerous studies have linked exposure to air pollution with an increased likelihood of autism. These associations have been reported across multiple regions, including Asia (Chen et al., 2018; Li et al., 2026), Europe (Flanagan et al., 2023; Jin et al., 2024), and North America (Cloutier et al., 2025; Volk et al., 2013). Most of this research has focused on PM_2.5 and other common traffic-related pollutants. As expected in complex human studies, results vary across populations and methodologies, but the overall pattern of findings points in a consistent direction.

As the research has matured, investigators have begun asking more refined questions. Does particle size matter? Are smaller particles more biologically active? Are there specific windows of vulnerability? Recent work, including analyses from the Childhood Autism Risk from Genetics and the Environment study, suggests that exposure to ultrafine particles during early childhood may be particularly relevant (Goodrich et al., 2024).

This shift toward greater precision mirrors the broader evolution of autism research. Early work identifies associations. Later work clarifies timing, mechanisms, and susceptibility. ARI has encouraged this kind of careful progression from the beginning.

How to prepare for PM exposure in early life

Just as pregnant women are advised to avoid alcohol, cigarette smoke, pumping gasoline into their cars, and other toxic exposures, future public health recommendations may also include guidance related to air pollution. Such recommendations, potentially informed by statistical models, could take into account factors such as proximity to major roads or highways, distance from heavy traffic, and even temperature, since particulate matter can remain suspended in the air longer during warmer conditions (Leffel et al., 2025).

For individuals who live in or spend substantial time in high PM environments, protective strategies may begin as early as preconception and continue through pregnancy and early childhood. These strategies could include using air purifiers in the home and workplace, wearing masks outdoors when pollution levels are elevated, and taking additional precautions to reduce exposure during a child’s early years. Other approaches may involve targeted nutritional supplementation aimed at supporting cellular resilience and detoxification pathways.

As discussed in a previous editorial, the P2i program offers a comprehensive training framework for healthcare providers and families preparing for pregnancy or welcoming a new child, with the goal of reducing overall toxic burden. (See www.forump2i.com.)

Continuing ARI’s legacy of careful, pattern-based inquiry

As always, caution is essential. None of the conditions discussed above are caused by any single mechanism. Autism is certainly not caused by any single factor. Many autistic people are happy being autistic and see autism as part of neurodiversity, meaning all brains are different.  Genetics, immune function, metabolism, and environment all play roles. The current research does not suggest that particulate matter causes autism. What it does show is biological plausibility of how pollution is impacting human experience.

ARI has long emphasized that progress in autism research comes from recognizing patterns early and evaluating them carefully over time. The growing evidence linking particulate matter to neurodevelopmental vulnerability fits this pattern. These exposures are widespread, largely invisible, and part of daily life.

As research advances, the most important questions may shift. Rather than asking whether particulate matter matters at all, the focus may need to move to when it matters most, how it interacts with underlying biology, and which individuals are most vulnerable. These differences likely reflect epigenetic and biological variability, since not everyone exposed to particulate matter experiences adverse effects. Addressing these questions aligns closely with ARI’s longstanding mission to integrate research, clinical insight, and real-world relevance.

This editorial is available in PDF format – Download Here
References are available at www.ARRIReferences.org.
This article originally appeared in Autism Research Review International, Vol. 40, No. 1, 2026

Connie Kasari, PhD, details what contemporary research reveals about supporting non-speaking or minimally verbal autistic children. She highlights how far the field has come in the past two decades and emphasizes the need for contemporary research to focus on what strategies benefit whom and why. The speaker discusses JASPER, a modular intervention based on social communication. She outlines recent studies and video examples showing positive language outcomes for JASPER on its own and in tandem with other interventions. Kasari underscores the usefulness of AAC devices in spoken language development, noting the lack of interventions that use even low-tech augmentative supports. The speaker summarizes her presentation and focus for future research before the Q&A.

Handouts are online HERE

In this webinar

2:00 – Early intervention in autism
7:00 – Core challenges: Video
14:16 – Study: JASPER intervention outcomes
26:00 – Intervention trajectories
31:50 – Study: Intervention combinations and AAC
36:11 – Implications for practice
45:45 – AAC case studies
46:45 – Summary
48:00 – Q&A

Early intervention and social communication

Kasari explains that nearly all autistic children will require support/intervention on engagement, imitation, joint attention, and play (2:00). She states that the goal of early intervention is to reduce the number of autistic children who have significant language impairment by the time they start school. Language ability remains one of the strongest predictors of positive long-term outcomes, making support strategies that target social communication skills—such as joint attention, engagement, and play—especially critical (4:00). Importantly, Kasari notes that research hasn’t focused on for whom an intervention works or why a particular intervention provides benefit for certain people. Understanding this is critical to expanding care and assessment across the board (5:30).

The speaker discusses core challenges that may trigger an intervention and shows videos comparing social communication in an autistic and a non-autistic child at 18 months old. Kasari highlights differences between the videos, noting the child with autism is more interested in looking at the objects than communicating (7:00). She explains how this pattern often translates to parent play, making it feel frustrating or not enjoyable for many parents/caregivers, and discusses two video examples of this (9:30).

Social Communication Research

The speaker says we know the least about children who are most delayed in development, who have limited language skills, and those whose families have less access to information about studies in their communities. She explains that most autistic children have never been in a research study. As a result, our evidence base does not represent the entire spectrum of autism (13:15). Kasari and her team focus on researching interventions for non-speaking and minimally verbal autistic children that can be conducted in community settings.

JASPER: Joint Attention, Symbolic Play, Engagement, and Regulation

The presenter describes JASPER, a comprehensive social communication/language intervention that can float inside other interventions, be used on its own or used sequentially (14:60). Kasari presents one of her recent publications comparing outcomes in 164 children, 3 -5 years old, across three sites after four months receiving Discrete Trial Training (DTT) or JASPER (video examples) (19:00). Results from the study show that both groups made significant language gains, and 45% moved toward phrased speech (putting words together).

Intervention trajectories

The goal of the intervention was to avoid the label of minimally verbal or profound autism by school age. Kasari defines profound autism as children with a developmental quotient (DQ) below 50, aged 8 or older, with poor adaptive skills (often minimally verbal or non-speaking). She notes that this is a relatively new term and considers how early we can predict these outcomes (26:00). The speaker reviews DQ data for a group of 264 children at very young ages. By age 8, 47% did not meet criteria for profound autism, although 25% of this group had a DQ lower than 50 at age 4 (28:30).

Kasari summarizes study takeaways, noting that DQ can help predict later development but is not a perfect predictor on its own. She reiterates the importance of early intervention and highlights understanding the 25% who moved off trajectory as a critical next step (29:25).

Combination interventions and assistive technology (AAC)

The presenter reiterates the heterogeneity in response to interventions, underscoring the need to personalize, tailor, and target interventions according to each person. This will also help us address for whom the intervention works and why. Kasari defines adaptive intervention designs as a sequence of decision rules that specify whether, how, when (timing), and based on which measures, to alter the dosage (duration, frequency, or amount), type, or delivery of treatment(s) at decision stages in the course of care – this is what her group employs (29:45).

Kasari details a study with 61 children, 5-8 years old, who are minimally verbal and had received 2 years of intensive early intervention (most ABA). All children received JASPER plus EMT, a spoken language intervention. Half of the children were randomized to receive AAC devices to test if these supports help with spoken language. Children attended two sessions per week, and at the 12-week follow-up, those assessed as slow responders were re-randomized to either add AAC or to up to 3 sessions per week. Outcomes for socially communicative utterances were assessed after another 12 weeks (31:50). Those who used AAC devices from the beginning showed significant increases and also had more novel words and joint attention language. Those with only JASPER and EMT made slow but steady progress. Researchers also found that from entry to midpoint to exit, parent-initiated engagement stayed the same while child-initiated engagement increased (34:15).

Implications for practice

The speaker notes that assistive technology are still not used regularly with children, be it a device, sign language, or another low-tech augmentative device; they are not being used as much as they should (36:11). Kasari returns to the child from the first video and describes how they changed tactics the second day by lowering the play level and adding an AAC device with button-words (video provided) (40:00). She notes that this child entered regular education at age 7, speaking full sentences. He used the AAC for a few years as a transition to spoken language. The presenter describes another case in which a child used AAC to support communication. He made progress over time, eventually asking the therapist to put phrases that he hears in the AAC device so he can listen to them and learn the sounds. In a follow-up video, the child is speaking in full sentences (45:45).

Kasari summarizes her presentation, highlighting that we can improve social communication and language outcomes for delayed autistic children and that these early skills need to be direct targets for support/intervention strategies. She reiterates how research must inform practice and, therefore, focus on answering questions about personalized interventions (how long do we wait, what do we change to?) (46:45) before the Q&A (48:00).