Association of Pulmonary Functions with Motor and Sensory Nerve Conduction Study in Smokers

ABSTRACT

Background:

The tobacco epidemic is one of the greatest hazards to public health that the world has ever encountered.

Objective:

To evaluate correlation of neuropathy with advanced airflow obstruction due to chronic smoking.

Materials and Methods:

This research was conducted on 40 healthy male smokers and 40 healthy nonsmokers. Pulmonary function test was performed in all subjects with computerized spirometer (Spiro Excel—software version 1.1), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow rate, FEV1/FVC were recorded. Nerve conduction studies were performed using Neuroperfect Machine—”EMG, NCV, EP—Medicaid Machine 2000.” Both the upper limbs and both lower limbs were tested for motor and sensory nerves study.

Results and Conclusion:

Frank neuropathy is not observed in healthy adult male smokers, but the dysfunction of peripheral nerves is observed and dysfunction increases as the pulmonary functions deteriorate. It was concluded that long before the emergence of clinical neuropathy, the deterioration in nerves and even lung functions could be diagnosed earlier by electrophysiological studies.

INTRODUCTION

The tobacco epidemic is one of the greatest hazards to public health that the world has ever encountered.[1] Toxic mixtures of over 7,000 chemicals make up tobacco smoke. We all are aware about the ill effects of cigarette smoking, especially on lung functions. But there are many systemic effects that are not studied in depth-like effect of smoking on nerve functions. Chronic hypoxemia caused by deteriorated lung functions is known to cause neuropathy in chronic obstructive pulmonary disease (COPD) patients as per previous studies and correlation of neuropathy is significantly seen with higher consumption of cigarettes in COPD patients. A significant correlation of neuropathy with advanced airflow obstruction in terms of reduction in forced expiratory volume in one second (FEV1%) and peak expiratory flow rate (PEFR) has also been observed in COPD patients. We can identify the tip of iceberg by studying the correlation of deterioration in lung function in apparently healthy young adult male smokers.[2]

This study was done to evaluate correlation of neuropathy with advanced airflow obstruction due to chronic smoking.

MATERIALS AND METHODS

This study was conducted at the Department of Physiology’s electrophysiology lab at the People’s College of Medical Sciences and Research Centre in Bhopal, Madhya Pradesh. After rigorous selection based on inclusion and exclusion criteria, the study was conducted on 40 male smokers who appeared to be in good health and 40 nonsmokers who appeared to be in good health and were employed by different People’s University constituent institutions. The participants were between the ages of 20 and 40. After taking into account the inclusion and exclusion criteria, the study was completed.

To evaluate the severity of smoking, both in terms of length and average daily cigarette use, smokers were categorized based on their smoking index.

Smokers were divided into the following categories based on the smoking index:

• Group 1. Light smokers: smoking index <100

• Group 2. Moderate smokers: smoking inde × 101–200

• Group 3. Heavy smokers: smoking index >200

• Group 4: Nonsmokers

The nonsmoker group was made up of healthy individuals in the 20–40 age range who had never smoked, had no other tobacco-related exposures (such as tobacco chewing, gutakha, pan masala, mishri, etc.), and had no history of serious illness or substance abuse that resulted in peripheral neuropathy.

Pulmonary function test was performed in all subjects with computerized spirometer into the premedicated spirometry mouthpiece which was connected to computer software. The flow, volume/timed graphs were recorded in accordance to the criteria based on the American Thoracic Society and the best of the three acceptable curves were selected for further analysis. Forced vital capacity (FVC), FEV₁, FEV₁/FVC ratio and PEFR were recorded:

Nerve conduction studies were done using Neuroperfect Machine—”EMG, NCV, EP—Medicaid Machine 2000.” Both the upper limbs and lower limbs were tested for motor and sensory nerves study. The important nerves tested are as follows:

For motor nerve conduction study, stimulation was given on the concerned nerve (e.g. median nerve at wrist) and compound muscle action potential (CMAP) was recorded. Then amplitude and latency were measured by marking the point of stimulus, onset, offset baseline and peak of CMAP, and nerve conduction velocity was measured by the formula:

A stimulus was applied proximally to the nerve in order to provide an antidromic measurement for the sensory nerve conduction investigation. Amplitude, latency, and NCV were measured after a sensory nerve action potential was captured.

RESULTS

The data were statistically evaluated by SPSS software version 21.0 (IMB, Chicago, USA) with one-way ANOVA test. Table 1 shows that all parameters, FEV1, FVC, FEV1/FVC, and PEFR, were highly significantly different (P < 0.001) among all the groups. Table 2 shows how smoking affects the study of motor nerve conduction in the upper and lower limbs. Table 3 shows how smoking affects the investigation of sensory nerve conduction in the upper and lower limbs.

Table 1.

Effect of smoking on pulmonary function test

Parameter	Group 1 Light smoker	Group 2 Moderate smoker	Group 3 Heavy smoker	Group 4 Nonsmoker	ANOVA (F)	P
FEV1% predicted	73.71±1.06	69.61±2.44	53.11±1.10	89.15±2.35	940.695	0.001 (HS)
FVC% predicted	90.01±1.59	87.02±1.4	68.13±1.46	90.04±3.28	156.82	0.001 (HS)
FEV1/FVC%	81.82±0.92	79.97±1.5	73.048±2.34	96.67±5.46	136.952	0.001 (HS)
PEFR% predicted	71.55±1.34	67.85±1.64	61.61±0.87	86.19±1.784	619.108	0.001 (HS)

HS=highly significant, PEFR=peak expiratory flow rate, FVC=forced vital capacity, FEV1=forced expiratory volume in 1 s

Table 2.

Impact of smoking on upper and lower limb motor nerve conduction research

Parameter	Group 1 Light smoker	Group 2 Moderate smoker	Group 3 Heavy smoker	Group 4 Nonsmoker	ANOVA (F)	P
MNCV (m/s)	54.49±1.46	51.26±1.65	49.76±0.49	60±6.47	25.346	0.01 (S)
CMAP (µV)	6.28±2.21	6.18±1.72	5.21±1.23	7.45±3.26	249	0.01 (S)
DL-Motor (s)	3.04±1.12	3.31±1.03	4.54±0.78	2.76±1.07	400	0.001 (HS)

Values expressed as mean±standard deviation. HS=highly significant, S=significant, CMAP=compound muscle action potential, MNCV=motor nerve conduction velocity

Table 3.

Smoking’s effects on upper and lower limb sensory nerve conduction studies

Parameter	Group 1 Light smoker	Group 2 Moderate smoker	Group 3 Heavy smoker	Group 4 Nonsmoker	ANOVA (F)	P
SNCV (m/s)	76.65±2.18	68.76±2.07	66.26±5.68	92.40±7.37	104.72	0.001 (HS)
SNAP (µV)	42.24±12.5	22.88±11.57	18±7.6	51.37±17.13	144	0.01 (S)
DL (sensory) (ms)	2.06±0.05	2.27±0.65	2.4±0.069	1.74±0.57	1,877	0.001 (HS)

HS=highly significant, S=significant, SNCV=sensory nerve conduction velocity, SNAP=sensory nerve action potential

DISCUSSION

Like everywhere else, tobacco use and smoking, in particular, are the leading preventable causes of death for adults in India.[3] The purpose of this study is to raise awareness among young smokers who are only beginning to explore the extent of the problem.

FEV1 reduction is one of the early determinants of pulmonary dysfunction in apparently healthy smokers. Prolongation of distal latency of sensory nerves in light smokers reveals that changes in myelin sheath occur slowly at very early age although it may take years to affect the conduction velocity in smokers. Slowly progressive demyelination process affects sensory nerves.[4]

In moderate smokers, there is 21% fall in FEV1, 3% fall in FVC, 17% fall in FEV1/FVC, and 21% fall in PEFR. The fall in FEV1 is greater than fall in FVC values which is indicative of obstructive lung dysfunction.

Obstructive lung dysfunction in moderate smokers leads to hypoxia. The highly significant positive correlation of MNCV and CMAP is seen with all the parameters of the pulmonary function test in heavy smokers while distal latency of motor nerves shows highly significant negative correlation with all the parameters of pulmonary function test (PFT).

Among the sensory nerve conduction study, SNCV shows a highly significant and positive correlation with all the parameters of PFT. Also, the distal latency of sensory nerves is correlated negatively with all the parameters of PFT and association shown is highly significant. Our findings in heavy smokers are justified by the study by Rimer et al.[5]

Peripheral neuropathy is known to be caused by chronic hypoxemia.[6] Nerve conduction velocity slows down in animal models of persistent hypoxemia. As a process that requires energy, axonal transport can be hampered by hypoxemia, which can worsen axonal degeneration.[5] One significant contributing factor to the development of peripheral neuropathy associated with COPD may be cigarette smoking.[6]

CONCLUSION

Although all of the MNCS and SNCS values in our study are within the normal range, they are significantly lower than those of the nonsmoker group. This result is consistent with research by Agrawal et al., who discovered subclinical neuropathy in patients with stable COPD.[7]

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.