Influence of coal-derived air pollutants on cognitive and neurobehavioral function among children
Authors
- Haripratha SaravananDepartment of Physiotherapy, School of Physiotherapy, Sri Balaji Vidyapeeth, Puducherry, India
- S. Kiran KumarDepartment of Physiotherapy, Peri College of Physiotherapy, Manivakkam, Chennai, India
- Gopal NambiDepartment of Health and Rehabilitation Sciences, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia
- Shanmugananth ElayaperumalDepartment of Physiotherapy, School of Physiotherapy, Sri Balaji Vidyapeeth, Puducherry, India
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Published by Bangladesh Medical University (former Bangabandhu Sheikh Mujib Medical University).
Fine Fine particulate matter is one of the leading causes of ambient air pollution that threatens the global public health. About seven million premature deaths occur annually in low- and middle-income countries [1]. Among all air pollutants, coal dust arising from the processes of coal extraction, storage, and combustion, with the fine particles generated during coal mining, contributes to major personal health and occupational-related complications [2]. Burned coal produces a waste by-product known as coal ash which is a major component and inhalable particulate matter ranging in diameter from 0.1 μm to >10 μm [3]. The fly ash consisted of concentrated metal (loids), approximately 2 –10 times more concentrated than the parent coal and found that concentration of lead in coal fly ash was 35 (parts per million) ppm compared to only 4 ppm in parent coal [4].
Long-term exposure to fine dust particles allows them to enter the lungs through nasal passages and penetrate the bloodstream, ultimately breaching the blood-brain barrier. These particles diffuse directly into the deep brain tissues via synaptic transmission. This process triggers an increase in beta-amyloid proteins, their precursor protein-cleaving enzymes, cyclooxygenase and pro-inflammatory cytokines, ultimately causing disruptive changes in brain networks [5]. The intensifying dust concentration produces atrophy in frontal lobe, parietal lobe, occipital lobe and internal capsule and significantly influences anomalies of brain and contributes to serious central nervous system disorders which mainly deteriorates to cognitive function such as memory, thought processes, spatial orientation, language abilities, social and judgmental capabilities [6].
A cross-sectional study conducted on 111 children aged between 4 to 17 years living adjacent to coal ash storages and a non – exposed area, found that the power plant was used since 1950 and burned 1.3 million tons of coal annually and coal ash components such as lead, mercury and arsenic induces severe adverse health outcomes affecting multiple organ systems and disrupts brain development which impairs cognitive function [7]. Comparing the relative studies impact of particulate matters from coal dust exposure is highly significant risk factor for cognitive decline. Hence, the objective of the present study was to assess the association between coal-derived air pollutants and cognitive as well as neurobehavioral function among children.
The community-based cross-sectional study was conducted in Cuddalore district, Tamil Nadu, India, between January 2026 and march 2026. A total of 190 were screened initially. Sample size estimation was performed using an assumed moderate effect size of 0.5, alpha level of 0.5 and statistical power of 80%. Children were recruited based on spelling and arithmetic (Teste do Desempenho Escolar) TDE subsets performance [8]. The TDE criterion was used to identify children with possible learning difficulties relevant to neurocognitive assessment. The inclusion criteria included school-aged children between 8 to 12 years, both males and females, residing near coal-fired power plant for at least 5 years, children scoring below 25th percentile on arithmetic and spelling TDE subtests, consent from anyone of the parents. The exclusion criteria included history of congenital impairment/ disorders, history of pre-mature birth and other neurological disorders. The samples were categorized into 2 groups based on the locality. Those who lived within 10 miles from coal-fired power plants taken as Group A and those who lived away from 40 miles were considered as Group B. These (10-mile and 40 mile) cut-off were selected to represent higher and lower environmental exposure zones based on regional particulate matter dispersion patterns reported in previous environmental studies. The autonomy, consent and child assent were obtained. The participants demographic details such as age, gender, home/residential address were evaluated.
The children satisfied the selection criteria were evaluated initially with TDE subsets and later, using Mini Mental state examination for children (MMS) [9] and child behavior checklist (CBCL) [10]. The air quality of the individual children locality was evaluated. The personal modular impactor was installed at representative monitoring locations within the study regions approximately one week prior to assessment to estimate ambient PM10 exposure levels [3]. Allocation was concealed. Data analyst was blinded.
Table 1 Comparison of cognitive and neurobehavioural symptoms between children residing near (Group A) and far (Group B) from coal-fired power plants
| Crude mean (standard deviation) |
| Adjusteda mean (standard deviation) | ||||
Group A | Group B | P | Group A | Group B | P | ||
MMS score | 26.8 (2.0) | 32.2 (2.9) | <0.001 |
| 26.9 (0.3) | 32.3 (0.3) | <0.001 |
CBCL score | 65.7 (2.0) | 62.4 (3.9) | <0.001 | 65.8 (0.4) | 62.5 (0.4) | <0.001 | |
MMS indicates Mini-Mental State examination for children; CBCL, Child Behaviour Checklist; Group A, those who live within 10 miles and Group B, 40 miles perimeter of the coal mines. aData were adjusted for the age and sex of the participants. | |||||||
Data were analyzed using R programming language. Descriptive statistics were summarized using mean and standard deviation. The welch two sample t-test were used to compare outcome measures between groups. A coefficient of variation was utilized to identify the consistency of the data sets. Of the 190 participants initially screened, 115 participants met the final eligibility criteria and completed all assessments (Group A = 61; Group B = 54). The remaining participants were excluded due to incomplete assessments, failure to meet eligibility criteria or withdrawal of consent. The current study focused on analyzing the cognitive function using mini mental state examination, which resulted that participants in group A 26.9 (2.0) have higher cognitive deficits compared to group B 32.3 (2.9) (P <0.001). Greater changes were found in the neuro-behavioral symptoms of group A score 65.8 (2.1) compared to group B score 62.4 (3.9) (P <0.001). The effect size, 1.1, was statistically significant (95% confidence interval, 2.1-4.5). It is hypothesized that the children who were residing near the coal emission areas will have higher susceptibility for disruption in brain development and cognitive impairment. These findings are consistent with previous international studies reporting associations between particulate matter exposure and adverse neurocognitive outcomes in children.


Variables | Frequency (%) |
Indication of colposcopy |
|
Visual inspection of the cervix with acetic acid positive | 200 (66.7) |
Abnormal pap test | 13 (4.3) |
Human papilloma virus DNA positive | 4 (1.3) |
Suspicious looking cervix | 14 (4.7) |
Others (per vaginal discharge, post-coital bleeding) | 69 (23.0) |
Histopathological diagnosis | |
Cervical Intraepithelial Neoplasia 1 | 193 (64.3) |
Cervical Intraepithelial Neoplasia 2 | 26 (8.7) |
Cervical Intraepithelial Neoplasia 3 | 32 (10.7) |
Invasive cervical cancer | 27 (9.0) |
Chronic cervicitis | 17 (5.6) |
Squamous metaplasia | 5 (1.7) |
Groups based on pre-test marks | Pretest | Posttest Marks (%) | Difference in pre and post-test marks (mean improvement) | P |
Didactic lecture classes | ||||
<50% | 36.6 (4.8) | 63.2 (9.4) | 26.6 | <0.001 |
≥50% | 52.8 (4.5) | 72.4 (14.9) | 19.6 | <0.001 |
Flipped classes | ||||
<50% | 36.9 (4.7) | 82.2 (10.8) | 45.4 | <0.001 |
≥50% | 52.8 (4.6) | 84.2 (10.3) | 31.4 | <0.001 |
Data presented as mean (standard deviation) | ||||
Background characteristics | Number (%) |
Age at presentation (weeks)a | 14.3 (9.2) |
Gestational age at birth (weeks)a | 37.5 (2.8) |
Birth weight (grams)a | 2,975.0 (825.0) |
Sex |
|
Male | 82 (41) |
Female | 118 (59) |
Affected side |
|
Right | 140 (70) |
Left | 54 (27) |
Bilateral | 6 (3) |
Delivery type |
|
Normal vaginal delivery | 152 (76) |
Instrumental delivery | 40 (20) |
Cesarean section | 8 (4) |
Place of delivery |
|
Home delivery by traditional birth attendant | 30 (15) |
Hospital delivery by midwife | 120 (60) |
Hospital delivery by doctor | 50 (25) |
Prolonged labor | 136 (68) |
Presentation |
|
Cephalic | 144 (72) |
Breech | 40 (20) |
Transverse | 16 (8) |
Shoulder dystocia | 136 (68) |
Maternal diabetes | 40 (20) |
Maternal age (years)a | 27.5 (6.8) |
Parity of mother |
|
Primipara | 156 (78) |
Multipara | 156 (78) |
aMean (standard deviation), all others are n (%) | |
Background characteristics | Number (%) |
Age at presentation (weeks)a | 14.3 (9.2) |
Gestational age at birth (weeks)a | 37.5 (2.8) |
Birth weight (grams)a | 2,975.0 (825.0) |
Sex |
|
Male | 82 (41) |
Female | 118 (59) |
Affected side |
|
Right | 140 (70) |
Left | 54 (27) |
Bilateral | 6 (3) |
Delivery type |
|
Normal vaginal delivery | 152 (76) |
Instrumental delivery | 40 (20) |
Cesarean section | 8 (4) |
Place of delivery |
|
Home delivery by traditional birth attendant | 30 (15) |
Hospital delivery by midwife | 120 (60) |
Hospital delivery by doctor | 50 (25) |
Prolonged labor | 136 (68) |
Presentation |
|
Cephalic | 144 (72) |
Breech | 40 (20) |
Transverse | 16 (8) |
Shoulder dystocia | 136 (68) |
Maternal diabetes | 40 (20) |
Maternal age (years)a | 27.5 (6.8) |
Parity of mother |
|
Primipara | 156 (78) |
Multipara | 156 (78) |
aMean (standard deviation), all others are n (%) | |
Mean escape latency of acquisition day | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
Days |
|
|
|
|
|
1st | 26.2 (2.3) | 30.6 (2.4) | 60.0 (0.0)b | 43.2 (1.8)b | 43.8 (1.6)b |
2nd | 22.6 (1.0) | 25.4 (0.6) | 58.9 (0.5)b | 38.6 (2.0)b | 40.5 (1.2)b |
3rd | 14.5 (1.8) | 18.9 (0.4) | 56.5 (1.2)b | 34.2 (1.9)b | 33.8 (1.0)b |
4th | 13.1 (1.7) | 17.5 (0.8) | 53.9 (0.7)b | 35.0 (1.6)b | 34.9 (1.6)b |
5th | 13.0 (1.2) | 15.9 (0.7) | 51.7 (2.0)b | 25.9 (0.7)b | 27.7 (0.9)b |
6th | 12.2 (1.0) | 13.3 (0.4) | 49.5 (2.0)b | 16.8 (1.1)b | 16.8 (0.8)b |
Average of acquisition days | |||||
5th and 6th | 12.6 (0.2) | 14.6 (0.8) | 50.6 (0.7)b | 20.4 (2.1)a | 22.4 (3.2)a |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.05; bP <0.01. | |||||
Categories | Number (%) |
Sex |
|
Male | 36 (60.0) |
Female | 24 (40.0) |
Age in yearsa | 8.8 (4.2) |
Education |
|
Pre-school | 20 (33.3) |
Elementary school | 24 (40.0) |
Junior high school | 16 (26.7) |
Cancer diagnoses |
|
Acute lymphoblastic leukemia | 33 (55) |
Retinoblastoma | 5 (8.3) |
Acute myeloid leukemia | 4 (6.7) |
Non-Hodgkins lymphoma | 4 (6.7) |
Osteosarcoma | 3 (5) |
Hepatoblastoma | 2 (3.3) |
Lymphoma | 2 (3.3) |
Neuroblastoma | 2 (3.3) |
Medulloblastoma | 1 (1.7) |
Neurofibroma | 1 (1.7) |
Ovarian tumour | 1 (1.7) |
Pancreatic cancer | 1 (1.7) |
Rhabdomyosarcoma | 1 (1.7) |
aMean (standard deviation) | |



Test results | Disease | Sensitivity (%) | Specificity (%) | PPV (%) | NPV (%) | ||
Yes | No | ||||||
Reid’s score ≥ 5 | Positive | 10 | 15 | 37.0 | 94.5 | 40.1 | 93.8 |
Negative | 17 | 258 |
|
|
|
| |
Swede score ≥ 5 | Positive | 20 | 150 | 74.1 | 45.0 | 11.8 | 94.6 |
Negative | 7 | 123 |
|
|
|
| |
Swede score ≥ 8 | Positive | 3 | 21 | 11.1 | 92.3 | 12.5 | 91.3 |
Negative | 24 | 252 |
|
|
|
| |
a High-grade indicates a score of ≥5 in both tests; PPV indicates positive predictive value; NPV, negative predictive value | |||||||
Test | Sensitivity (%) | Specificity (%) | Positive predictive value (%) | Negative predictive value (%) |
Reid’s score ≥ 5 | 37.0 | 94.5 | 40.0 | 93.8 |
Swede score ≥ 5 | 74.1 | 45 | 11.8 | 94.6 |
Swede score ≥ 8 | 11.1 | 92.3 | 12.5 | 91.3 |
Test | Sensitivity (%) | Specificity (%) | Positive predictive value (%) | Negative predictive value (%) |
Reid’s score ≥ 5 | 37.0 | 94.5 | 40.0 | 93.8 |
Swede score ≥ 5 | 74.1 | 45 | 11.8 | 94.6 |
Swede score ≥ 8 | 11.1 | 92.3 | 12.5 | 91.3 |
Narakas classification | Total 200 (100%) | Grade 1 72 (36%) | Grade 2 64 (32%) | Grade 3 50 (25%) | Grade 4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7, 8, 9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Narakas classification | Total 200 (100%) | Grade-1 72 (36%) | Grade-2 64 (32%) | Grade-3 50 (25%) | Grade-4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7,8,9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Variables in probe trial day | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
Target crossings | 8.0 (0.3) | 7.3 (0.3) | 1.7 (0.2)a | 6.0 (0.3)a | 5.8 (0.4)a |
Time spent in target | 18.0 (0.4) | 16.2 (0.7) | 5.8 (0.8)a | 15.3 (0.7)a | 15.2 (0.9)a |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.01. | |||||
Pain level | Number (%) | P | ||
Pre | Post 1 | Post 2 | ||
Mean (SD)a pain score | 4.7 (1.9) | 2.7 (1.6) | 0.8 (1.1) | <0.001 |
Pain categories | ||||
No pain (0) | - | 1 (1.7) | 31 (51.7) | <0.001 |
Mild pain (1-3) | 15 (25.0) | 43 (70.0) | 27 (45.0) | |
Moderete pain (4-6) | 37 (61.7) | 15 (25.0) | 2 (3.3) | |
Severe pain (7-10) | 8 (13.3) | 2 (3.3) | - | |
aPain scores according to the visual analogue scale ranging from 0 to 10; SD indicates standard deviation | ||||
Surgeries | Number (%) | Satisfactory outcomes n (%) |
Primary surgery (n=24) |
|
|
Upper plexus | 6 (25) | 5 (83) |
Pan-palsy | 18 (75) | 6 (33) |
All | 24 (100) | 11 (46) |
Secondary Surgery (n=26) |
|
|
Shoulder deformity | 15 (58) | 13 (87) |
Wrist and forearm deformity | 11 (42) | 6 (54) |
All | 26 (100) | 19 (73) |
Primary and secondary surgery | 50 (100) | 30 (60) |
Mallet score 14 to 25 or Raimondi score 2-3 or Medical Research grading >3 to 5. | ||
Narakas classification | Total 200 (100%) | Grade-1 72 (36%) | Grade-2 64 (32%) | Grade-3 50 (25%) | Grade-4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7,8,9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Trials | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
1 | 20.8 (0.6) | 22.1 (1.8) | 41.1 (1.3)b | 31.9 (1.9)b | 32.9 (1.8)a, b |
2 | 10.9 (0.6) | 14.9 (1.7) | 37.4 (1.1)b | 24.9 (2.0)b | 26.8 (2.5)b |
3 | 8.4 (0.5) | 9.9 (2.0) | 32.8 (1.2)b | 22.0 (1.4)b | 21.0 (1.4)b |
4 | 7.8 (0.5) | 10.4 (1.3) | 27.6(1.1)b | 12.8 (1.2)b | 13.0 (1.4)b |
Savings (%)c | 47.7 (3.0) | 33.0 (3.0) | 10.0 (0.9)b | 23.6 (2.7)b | 18.9 (5.3)b |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.05; bP <0.01. cThe difference in latency scores between trials 1 and 2, expressed as the percentage of savings increased from trial 1 to trial 2 | |||||


Lesion-size | Histopathology report | Total | |||||
CIN1 | CIN2 | CIN3 | ICC | CC | SM | ||
0–5 mm | 73 | 0 | 0 | 0 | 5 | 5 | 83 |
6–15 mm | 119 | 18 | 1 | 4 | 0 | 0 | 142 |
>15 mm | 1 | 8 | 31 | 23 | 12 | 0 | 75 |
Total | 193 | 26 | 32 | 27 | 17 | 5 | 300 |
CIN indicates cervical intraepithelial neoplasia; ICC, invasive cervical cancer; CC, chronic cervicitis; SM, squamous metaplasia | |||||||
| Histopathology report | Total | ||||||
CIN1 | CIN2 | CIN3 | ICC | CC | SM | |||
Lesion -Size | 0-5 mm | 73 | 0 | 0 | 0 | 5 | 5 | 83 |
6-15 mm | 119 | 18 | 1 | 4 | 0 | 0 | 142 | |
>15 mm | 1 | 8 | 31 | 23 | 12 | 0 | 75 | |
Total | 193 | 26 | 32 | 27 | 17 | 5 | 300 | |
CIN indicates Cervical intraepithelial neoplasia; ICC, Invasive cervical cancer; CC, Chronic cervicitis; SM, Squamous metaplasia | ||||||||
Group | Didactic posttest marks (%) | Flipped posttest marks (%) | Difference in marks (mean improvement) | P |
<50% | 63.2 (9.4) | 82.2 (10.8) | 19.0 | <0.001 |
≥50% | 72.4 (14.9) | 84.2 ( 10.3) | 11.8 | <0.001 |
Data presented as mean (standard deviation) | ||||








